Two Pediatric Cases of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Predominantly Presenting as Cortical Encephalitis: A Case Report and Literature Review

Two Pediatric Cases of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Predominantly Presenting as Cortical Encephalitis: A Case Report and Literature Review | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Two Pediatric Cases of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Predominantly Presenting as Cortical Encephalitis: A Case Report and Literature Review Jingbo Ma, Lei Sun, Lin Zhang, Xiaoyue Hu, Lijiao Fu, Ying Hua This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-9128341/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 7 You are reading this latest preprint version Abstract Objective To analyze and summarize the clinical characteristics of pediatric patients with myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) presenting with cortical encephalitis as the predominant clinical phenotype, thereby enhancing clinical awareness and facilitating early diagnosis and treatment. Methods We retrospectively analyzed the clinical data of two pediatric MOGAD cases with a predominant cortical encephalitis phenotype admitted to Wuxi Children's Hospital from March 2024 to March 2025. Their clinical presentations, treatments, and prognoses were summarized alongside a relevant literature review. Results In Patient 1, the patient initially presented with convulsive status epilepticus (March 2024) and normal cranial MRI, diagnosed as "severe encephalitis." After initial improvement, follow-up MRI two months later revealed frontotemporal cortical swelling, followed by another episode of status epilepticus one week subsequently. At that time, CSF was positive for MOG-IgG (titer 1:1), but serum was negative. The patient improved with immunotherapy. In March of this year, despite being asymptomatic, routine MRI again showed frontotemporal cortical swelling, and serum MOG-IgG was positive (titer 1:10+; live CBA). Acute treatment included IVIG and pulsed steroids, and the patient is now maintained on corticosteroids and mycophenolate mofetil. Patient 2 presented with prolonged fever,convulsions, headache, vomiting, and limb numbness. Serum MOG-IgG titer was 1:100+ (CBA), and MRI showed diffuse cerebral cortical swelling. The patient improved following IVIG and pulsed steroid therapy. Neither patient had relapsed at the one-year follow-up. Conclusion Pediatric myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) can manifest as cortical encephalitis, typically presenting with core symptoms including fever, headache, and seizures. The cortical encephalitis phenotype of MOGAD is more commonly observed in older children. Patients generally respond well to acute-phase treatment with intravenous immunoglobulin (IVIG) and pulsed methylprednisolone; however, a subset may experience relapses, necessitating timely initiation of second-line immunosuppressive therapy. When neuroimaging reveals features suggestive of cortical encephalitis, MOG antibody testing should be performed to confirm the diagnosis, preferably using a live cell-based assay (CBA) which offers higher sensitivity. Cortical encephalitis Pediatric myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) Live cell-based assay (CBA) Figures Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Introduction Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is the most common type of idiopathic inflammatory demyelinating disorder of the central nervous system in children. The phenotypic spectrum of MOGAD is diverse, including optic neuritis, myelitis, acute disseminated encephalomyelitis, unifocal or multifocal cerebral lesions, brainstem or cerebellar involvement, and cerebral cortical encephalitis. Notably, cerebral cortical encephalitis represents a distinct phenotype of MOGAD (MOG-CCE), which is autoimmune-mediated and predominantly confined to the cerebral cortex [1–3] . The pathogenesis of MOG-CCE remains to be fully elucidated. Current research suggests that MOG-CCE is an autoimmune disease mediated by anti-MOG antibodies, involving the participation of both humoral and cellular immunity. The proposed mechanism is as follows: First, environmental factors such as viral infections may trigger the activation and differentiation of MOG-specific CD4 + T cells in peripheral lymphoid organs of genetically susceptible individuals [4] . Concurrently, B cells located in the periphery or within the central nervous system (CNS) may also become activated, differentiating into plasma cells and producing anti-MOG antibodies [4, 5] . These activated CD4 + T cells, potentially synergizing with anti-MOG antibodies, then traverse the compromised blood-brain barrier (BBB) to enter the CNS parenchyma. Pathological studies [5] have provided supporting evidence for this hypothesis, revealing extensive inflammatory cell infiltration dominated by CD4 + T cells (predominant) and CD20 + B cells within the brain lesions of MOG-CCE, along with the phenomenon of macrophages engulfing MOG antigens (MOG-laden macrophages). These activated T cells further amplify the local inflammatory response through cytokine release. Concurrently, the anti-MOG antibodies that have entered the CNS exert their pathogenic effects through various pathways. Both the cortex and subcortical white matter can be involved, leading to clinical symptoms such as seizures and headache [5] . In summary, the pathogenesis of MOG-CCE is a multifactorial process resulting from the synergistic effects of specific T cell activation, antibody production, BBB disruption, and antibody effector functions. Within this process, CD4 + T cell-driven cellular immunity likely plays an initial and central role, while antibodies primarily act as effector molecules. Since the first report of unilateral cortical encephalitis with positive anti-MOG antibodies in 2017 [6] , pediatric MOGAD cases have remained rare. Herein, we report two pediatric cases of MOG antibody-positive CCE along with a review of the literature, aiming to enhance the understanding of this disease among pediatric clinicians. Materials and methods To comprehensively delineate the clinical characteristics of MOG antibody-associated cerebral cortical encephalitis, we conducted a systematic literature search. The PubMed database was searched using the keywords "Myelin Oligodendrocyte Glycoprotein" and "Cerebral Cortical Encephalitis." The Wanfang Database and China National Knowledge Infrastructure (CNKI) were searched using the keywords "anti-myelin oligodendrocyte glycoprotein antibody" and "cortical encephalitis". A cumulative total of 24 pediatric cases of MOG antibody-associated cortical encephalitis were retrieved from the literature [7–15]. Including the two cases reported herein, a total of 26 patients were analyzed. The inclusion criteria were: (1) age less than 18 years; (2) detection of serum anti-MOG antibodies at a titer greater than 1:10 at least once during the disease course; (3) cranial magnetic resonance imaging (MRI) revealing abnormal hyperintense signals predominantly confined to the cerebral cortex or sulci; and (4) an initial diagnosis of MOG-associated cortical encephalitis. The clinical characteristics, neuroimaging findings, and laboratory results of the 26 patients are summarized as follows (Table 1 ). Table 1 Summary of clinical characteristics in 26 pediatric cases of MOG antibody-associated cortical encephalitis Basic clinical features n(%) Laboratory Findings, Treatment, and Outcomes n(%) Sex MOG Male 12(46.15) Negative 0(0.00) Female 14(53.84) Positive 26(100.00) Age Combined anti-NMDAR positivity[14, 15] 4(15.38) Preschool age(≤ 6) 2(7.69) Brain MRI School age(> 6) 24(92.31) Unilateral cortical involvement 20(76.92) Clinical Manifestations Bilateral cortical involvement 6(23.08) Seizures 19(73.08) Treatment Todd's paresis 5(19.23) Methylprednisolone pulse therapy 24(92.31) Status epilepticus 9(34.62) Intravenous immunoglobulin 18(69.23) Fever 13(50.00) Immunosuppressants 6(23.08) Headache 14(53.84) Outcomes Psychiatric symptoms 6(23.08) Relapse 9(34.62) Speech impairment 8(30.77) Sequelae 7(26.92) Visual disturbances 8(30.77) Death 0(0.00) Paralysis 11(42.31) Clinical data Patient 1: The patient was a female infant, born in June 2013 via full-term vaginal delivery (G1P1), with a birth weight of 3300 g. There was no history of neonatal asphyxia, and the Apgar scores were 10 at both 5 and 10 minutes. Her family history was unremarkable. Initial Presentation: At the age of 10 years and 9 months(on March 3, 2024), the patient was admitted to the Pediatric Intensive Care Unit (PICU) of Wuxi Children's Hospital due to "recurrent convulsions for over 1 hour, accompanied by fever and vomiting." Her body weight at admission was 39 kg. During her PICU stay(6 days), she received intravenous immunoglobulin (IVIG) at a dose of 20 g/day for 2 days, intravenous methylprednisolone sodium succinate for anti-inflammatory therapy (2 mg/kg/day every 12 hours), and anti-seizure treatment with midazolam, propofol, and levetiracetam. After clinical improvement six days later, she was transferred to the Neurology Department for further management. Electroencephalography (EEG) performed during hospitalization revealed slow background activity (Fig. 1 ). Cerebrospinal fluid (CSF) analysis upon admission showed a white blood cell count of 101 × 10⁶/L; a repeat CSF analysis 11 days later revealed a normalized white blood cell count of 6 × 10⁶/L. CSF biochemistry was normal on both occasions. Two cranial magnetic resonance imaging (MRI) scans (eight days apart) showed no significant abnormalities. She was discharged with a diagnosis of severe viral encephalitis. Upon discharge on March 15, she was prescribed oral levetiracetam (0.5 g twice daily), which was discontinued by her parents after one month, and a sequential course of oral prednisone for one month. A follow-up outpatient EEG two weeks later was normal. First Relapse: Two months later, the patient presented to the outpatient clinic of Wuxi Children's Hospital with "two episodes of vomiting accompanied by dizziness within one month." An electroencephalogram (EEG) on May 2 again revealed slow waves (Fig. 2 ). A follow-up cranial magnetic resonance imaging (MRI) scan on May 8 suggested "right temporal gyral swelling with abnormal signals" (Fig. 3 ), and hospital admission was scheduled accordingly. On May 11, the patient experienced a seizure episode while awake, characterized by generalized seizures lasting for over one hour, accompanied by a low-grade fever (peak 37.8°C). On the same day, she was brought by her parents to another hospital and admitted for treatment. During hospitalization, cerebrospinal fluid (CSF) analysis on May 12 revealed a white blood cell count of 36 × 10⁶/L, with normal CSF biochemistry. Serum testing for anti-MOG-IgG, anti-AQP4-IgG, and anti-GFAP-IgG was negative; however, CSF analysis was positive for anti-MOG-IgG at a titer of 1:1, while other antibodies were negative. The patient remained generally well during the first five days of hospitalization. On the afternoon of May 16, she experienced another seizure episode, characterized by focal seizures with left limb twitching. Therefore, a contrast-enhanced cranial MRI was performed on May 20, which revealed abnormal signals in the right temporal and frontal lobes. Contrast-enhanced MRI of the full spine and orbits showed no significant abnormalities. The diagnoses at that time were: 1. Central nervous system demyelinating disease (suspected MOGAD); 2. Convulsive status epilepticus. Treatment was initiated with intravenous methylprednisolone (900 mg/day for 3 days, followed by 450 mg/day for 3 days; body weight at that time was 45 kg) and oral levetiracetam (0.5 g twice daily) for seizure control. Upon discharge, the patient was continued on a sequential course of oral prednisone with monthly outpatient follow-up. A follow-up contrast-enhanced cranial MRI on October 15 showed "significant improvement in the right temporal gyral swelling and abnormal signals compared to previous imaging" (Fig. 4 ). Consequently, prednisone was tapered and discontinued after a total treatment duration of six months. Second Relapse: Four months after discontinuing prednisone, the patient was admitted to Wuxi Children's Hospital due to transient right limb twitching lasting half an hour, which occurred following an episode of anger. During this hospitalization, repeat cerebrospinal fluid (CSF) analysis and electroencephalography (EEG) were both normal. Cranial magnetic resonance imaging (MRI) performed on March 3, 2025, revealed "abnormal signals in the right frontal and temporal lobes," involving the same regions as observed in May 2024 (Fig. 5 ). A live cell-based assay (CBA) revealed a serum anti-MOG-IgG antibody titer of 1:10+. The patient was treated with intravenous immunoglobulin (IVIG) pulse therapy (400 mg/kg/day for 5 days) and methylprednisolone pulse therapy (20 mg/kg/day for 3 days), followed by oral mycophenolate mofetil (0.5 g twice daily). At the one-year follow-up, the patient has remained relapse-free to date. Patient 2: The patient was a female infant, born in July 2012 via full-term vaginal delivery (G2P2), with a birth weight of 3000 g. There was no history of neonatal asphyxia, and the Apgar scores were 10 at both 5 and 10 minutes. She has one healthy older brother, and her family history was unremarkable. From March 5 to March 14, 2025, the patient experienced two episodes of afebrile seizures characterized by rightward deviation of both eyes and bilateral twitching of the left upper limb, lasting 3 minutes and 1 minute respectively before spontaneously resolving. On March 12, she experienced a transient episode of sudden loss of sensation in the left upper limb lasting over ten minutes, followed by residual numbness in the left upper limb upon recovery, which resolved spontaneously after approximately one hour. The patient was subsequently admitted to a local hospital. During hospitalization, she developed a low-grade fever (peak approximately 38°C) and received anti-infective and corticosteroid therapy, after which the fever subsided and she was discharged. However, she continued to experience recurrent dizziness and low-grade fever following discharge. Starting March 25, she developed headache and vomiting. On April 1, she was admitted to the Department of Neurology at Wuxi Children's Hospital due to "recurrent low-grade fever for one month accompanied by convulsions, dizziness, and headache for one week." Cerebrospinal fluid (CSF) analysis performed upon admission (April 1) revealed a white blood cell count of 130 × 10⁶/L with normal CSF biochemistry. Serum testing for anti-MOG-IgG antibodies was positive at a titer of 1:100+, and CSF testing was positive at a titer of 1:10+. Cranial magnetic resonance imaging (MRI) performed on April 3 revealed abnormal signal intensity in the right frontal cortex (Fig. 6 ). Following admission, the patient received intravenous immunoglobulin (IVIG) pulse therapy (400 mg/kg/day for 5 days) and two courses of methylprednisolone pulse therapy (20 mg/kg/day for 3 days per course), with oral prednisone 60 mg daily for 4 days (body weight 52 kg) administered between the two pulse courses. Following clinical improvement, the patient was discharged on a sequential course of oral prednisone. During outpatient follow-up from June to August, she occasionally experienced transient visual phenomena described as hexagonal shapes, lasting several seconds and resolving spontaneously. At the one-year follow-up, she has remained relapse-free to date. Discussion This paper reports two cases of pediatric patients with MOG antibody-associated cerebral cortical encephalitis (MOG-CCE), which illustrate the typical clinical features of this condition in the pediatric population while also demonstrating clinical heterogeneity. Both patients presented with acute or subacute onset, with fever, seizures, and headache as the core symptoms [1, 16]. Brain magnetic resonance imaging (MRI) revealed characteristic focal cortical abnormalities on FLAIR sequences accompanied by swelling (localized in the right frontal-temporal lobe in patient 1 and the right frontal lobe in patient 2), consistent with previously described imaging features of MOG-CCE [1, 3, 17]. Diagnosis was confirmed in both cases by the presence of positive serum anti-MOG-IgG antibodies [2, 18], and both patients showed favorable responses to first-line immunotherapy (high-dose corticosteroids combined with intravenous immunoglobulin). However, notable differences were observed between the two cases. Patient 1 predominantly manifested with seizures and status epilepticus, whereas patient 2 presented with seizures, limb numbness, and recurrent low-grade fever. Although patient 2 exhibited higher anti-MOG-IgG antibody titers, no relapses occurred; conversely, patient 1 experienced recurrent episodes despite lower antibody titers. Based on these observations, we hypothesize that there is no significant correlation between anti-MOG-IgG antibody titers and the risk of relapse. However, previous studies have suggested that school-aged children with initial antibody titers exceeding 1:1280 (median age 10 years) have the highest probability of relapse within two years [19]. Based on the two cases reported in this study and a review of the literature, we summarized the clinical characteristics of 26 pediatric patients (aged < 18 years) with MOG-CCE. The following findings were observed. Regarding demographic features, this condition predominantly affects school-aged and older children, with 92.31% of patients being over 6 years of age. The male-to-female ratio was approximately equal. This age distribution differs from that of adult MOG-CCE, which, according to current literature, can occur across all age groups, ranging from young adults to the middle-aged and elderly [1, 4].Clinically, seizures were the most prominent and core symptom, occurring in 73.08% of the 26 patients, with nearly half of these (9/19) presenting with status epilepticus. The incidence of seizures was considerably higher than that of other symptoms (headache 53.84%, fever 50%), indicating a tendency toward severe manifestations during the acute phase of this condition. For school-aged children with new-onset seizures, MOGAD should be included in the primary differential diagnosis [1, 16, 22]. Among the 26 patients, 4 cases (15.38%) were positive for concomitant anti-NMDAR antibodies. One of these cases [14] did not exhibit typical clinical symptoms and imaging features of anti-NMDAR encephalitis [20, 21], while the remaining 3 cases presented with mild anti-NMDAR encephalitis symptoms, consistent with previous reports [22]. Regarding imaging characteristics, the majority of patients (76.92%) exhibited unilateral cerebral cortical involvement on neuroimaging, which is highly consistent with imaging findings reported in adult patients [3, 17]. This observation suggests that anti-MOG antibody testing should be performed promptly when a patient presents with unilateral cortical encephalitis.In terms of treatment, the majority of patients showed a favorable response to first-line immunotherapy during the acute phase (methylprednisolone pulse therapy 92.31%, IVIG 69.23%). However, the relapse rate was relatively high, reaching 34.62%, with 23.08% of patients requiring long-term immunosuppressive agents to control relapses. The two most commonly used immunosuppressants were rituximab and mycophenolate mofetil. Regarding prognosis, some patients experienced a relapsing disease course [23]; however, no fatalities occurred among the 26 MOG-CCE cases. Most patients achieved complete recovery, indicating a generally favorable prognosis. Sequelae were observed in 26.92% (7 cases) of patients, including two patients who regained most functions with only mild articulation difficulties [7, 10], two patients with mild visual disturbances [15], and three patients who developed recurrent secondary epilepsy [11, 12] along with cognitive impairment and motor function deficits [11]. Overall, the prognosis in this pediatric cohort was better than that reported in adult cases. Pediatric MOGAD is an autoimmune disorder predominantly affecting school-aged children, with acute seizures (often presenting as status epilepticus) as its core clinical manifestation and unilateral cortical involvement as a characteristic imaging feature. Diagnosis relies on the detection of specific anti-MOG antibodies, with the cell-based assay (CBA) being the recommended method. While patients generally respond well to immunosuppressive therapy during the acute phase, the condition carries a significant risk of relapse. A subset of patients requires long-term immunosuppressive treatment and may experience residual sequelae. Pediatric neurologists should enhance their awareness of this entity to facilitate early diagnosis and implement individualized long-term management strategies . Declarations Acknowledgments We would like to express our gratitude to the patients and their parents for providing the case data. Author contributions All authors meet the ICMJE authorship criteria.YH,JM designed the study. LZ, XH collected and analyzed the data. JM,LF drafted the manuscript. SL provided imaging images. All authors read and approved the final manuscript. Conflict of interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Ethics statement The studies involving humans were approved by Ethics board approval and consent was obtained for this work from the Ethics Committee at the Children’s Hospital of Jiangnan University,Wuxi, Jiangsu, China (Ethics Number: WXCH2025-11-173). Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Consent for publication Written informed consent for publication of the clinical details and clinical images was obtained from the the patient’s parent. A copy of the consent form is available for review by the Editor of this journal. References Shu H, Ding M, Shang P, Song J, Lang Y, Cui L. Myelin Oligodendrocyte Glycoprotein Antibody Associated Cerebral Cortical Encephalitis: Case Reports and Review of Literature. Front Hum Neurosci. 2022 Jan 3;15:782490. Fujimori J. [Anti-myelin oligodendrocyte glycoprotein antibody associated encephalitis]. Rinsho Shinkeigaku. 2020 Feb 27;60(2):117-119. Japanese. 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Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease. Front Neurol. 2023 Feb 28;14:1137998. Takai Y, Misu T, Kaneko K, Chihara N, Narikawa K, Tsuchida S, Nishida H, Komori T, Seki M, Komatsu T, Nakamagoe K, Ikeda T, Yoshida M, Takahashi T, Ono H, Nishiyama S, Kuroda H, Nakashima I, Suzuki H, Bradl M, Lassmann H, Fujihara K, Aoki M; Japan MOG-antibody Disease Consortium. Myelin oligodendrocyte glycoprotein antibody-associated disease: an immunopathological study. Brain. 2020 May 1;143(5):1431-1446. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Reviews received at journal 21 Apr, 2026 Reviewers agreed at journal 15 Apr, 2026 Reviewers invited by journal 09 Apr, 2026 Editor invited by journal 25 Mar, 2026 Editor assigned by journal 25 Mar, 2026 Submission checks completed at journal 25 Mar, 2026 First submitted to journal 15 Mar, 2026 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-9128341","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":623939551,"identity":"3537c6c3-4ef8-4727-b6b8-15da088abeca","order_by":0,"name":"Jingbo Ma","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA0klEQVRIiWNgGAWjYBACNmbmgw8+/pOo52dvPkCcFj72tmTDGWwWCZI9xxKI0yLHc8ZMmoetIsHgRo4BkQ6TSDCT4OGRyJNsyPl44w2DnZxuA2EtyRYSEhLF/AxnN1vOYUg2NjtAWMvBGwYGEowzG3u3SfMwHEjcRlhLYoNEQoIE44bDPM+I1MJzmEniwAGJxA3HeNiI1MLexmzY2CBhLNnDZmw5x4AIv8g38398/LehTo5f/vHDG28q7OQIakEBEjxERg2yFlJ1jIJRMApGwYgAAMdgP4dQDJ2YAAAAAElFTkSuQmCC","orcid":"","institution":"Affiliated Children's Hospital of Jiangnan University","correspondingAuthor":true,"prefix":"","firstName":"Jingbo","middleName":"","lastName":"Ma","suffix":""},{"id":623939552,"identity":"a041d9ff-1b52-46fd-a24f-9d00b1da943e","order_by":1,"name":"Lei Sun","email":"","orcid":"","institution":"Affiliated Children's Hospital of Jiangnan University","correspondingAuthor":false,"prefix":"","firstName":"Lei","middleName":"","lastName":"Sun","suffix":""},{"id":623939553,"identity":"e4a9c107-2184-4ad8-ab8e-4253d979c8d9","order_by":2,"name":"Lin Zhang","email":"","orcid":"","institution":"Affiliated Children's Hospital of Jiangnan University","correspondingAuthor":false,"prefix":"","firstName":"Lin","middleName":"","lastName":"Zhang","suffix":""},{"id":623939554,"identity":"81b5307c-d73d-4632-aee2-ba9ddaec8817","order_by":3,"name":"Xiaoyue Hu","email":"","orcid":"","institution":"Affiliated Children's Hospital of Jiangnan University","correspondingAuthor":false,"prefix":"","firstName":"Xiaoyue","middleName":"","lastName":"Hu","suffix":""},{"id":623939555,"identity":"03af8ad7-8a1d-42be-9d53-734966b08668","order_by":4,"name":"Lijiao Fu","email":"","orcid":"","institution":"Affiliated Women’s Hospital of Jiangnan University","correspondingAuthor":false,"prefix":"","firstName":"Lijiao","middleName":"","lastName":"Fu","suffix":""},{"id":623939556,"identity":"98126c86-fbd2-4113-8dc3-c11f20be2b2c","order_by":5,"name":"Ying Hua","email":"","orcid":"","institution":"Affiliated Children's Hospital of Jiangnan University","correspondingAuthor":false,"prefix":"","firstName":"Ying","middleName":"","lastName":"Hua","suffix":""}],"badges":[],"createdAt":"2026-03-15 11:53:13","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-9128341/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-9128341/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":107483102,"identity":"98a39591-bd2c-415f-98c4-634e4b5f0f26","added_by":"auto","created_at":"2026-04-22 02:26:19","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":272707,"visible":true,"origin":"","legend":"\u003cp\u003eVideo electroencephalography (EEG) performed on March 11, 2024, revealed asymmetry in background rhythms between the hemispheres, with the left occipital region showing 2-3 Hz activity versus the right occipital region showing 6-7 Hz activity. Bilateral sharp slow waves were observed in the anterior head regions, which were more pronounced on the left side.\u003c/p\u003e","description":"","filename":"floatimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-9128341/v1/09d79dbb6afd54aaf1378054.png"},{"id":107254005,"identity":"5b27be14-2774-4403-b07e-5f57b38d4eaa","added_by":"auto","created_at":"2026-04-19 11:59:21","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":158419,"visible":true,"origin":"","legend":"\u003cp\u003eElectroencephalography (EEG) performed on May 8, 2024, showing sharp slow waves in the right anterior temporal region and the frontal pole.\u003c/p\u003e","description":"","filename":"floatimage2.png","url":"https://assets-eu.researchsquare.com/files/rs-9128341/v1/c1a9ab6833433ea2a503515c.png"},{"id":107254001,"identity":"22d81d93-cadb-47f9-bb0c-259ba53aef5a","added_by":"auto","created_at":"2026-04-19 11:59:21","extension":"jpeg","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":331544,"visible":true,"origin":"","legend":"\u003cp\u003eBrain MRI performed on May 7, 2024, demonstrating gyral swelling and abnormal signal intensity in the right frontal-temporal region.\u003c/p\u003e","description":"","filename":"floatimage3.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-9128341/v1/e7524cf0d58f5c8ff4305c88.jpeg"},{"id":107254003,"identity":"6625f074-1ba4-4fa3-b477-05c4b347cb10","added_by":"auto","created_at":"2026-04-19 11:59:21","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":156890,"visible":true,"origin":"","legend":"\u003cp\u003eBrain MRI performed on October 15, 2024, demonstrating improvement (or resolution) of the previously observed abnormal signal intensity.\u003c/p\u003e","description":"","filename":"floatimage4.png","url":"https://assets-eu.researchsquare.com/files/rs-9128341/v1/901562fa1b32eb0d255eb26a.png"},{"id":107484610,"identity":"30d2b624-d234-437a-bbf1-bee9dd8180dc","added_by":"auto","created_at":"2026-04-22 02:32:30","extension":"jpeg","order_by":5,"title":"Figure 5","display":"","copyAsset":false,"role":"figure","size":326802,"visible":true,"origin":"","legend":"\u003cp\u003eBrain MRI performed on March 3, 2025, showing abnormal signal intensity in the right frontal-temporal lobe.\u003c/p\u003e","description":"","filename":"floatimage5.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-9128341/v1/7e97a85d6ba3fed63b245c43.jpeg"},{"id":107484518,"identity":"9f535c95-c29d-4f9f-90e9-135a8d616675","added_by":"auto","created_at":"2026-04-22 02:32:12","extension":"jpeg","order_by":6,"title":"Figure 6","display":"","copyAsset":false,"role":"figure","size":277756,"visible":true,"origin":"","legend":"\u003cp\u003eMRI showing abnormal signal intensity in the right frontal lobe cortex.\u003c/p\u003e","description":"","filename":"floatimage6.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-9128341/v1/147cdc6a1d9eabc1f2a1f9cb.jpeg"},{"id":107487023,"identity":"b8ec8bed-7985-4012-a92e-b706f45a3fdf","added_by":"auto","created_at":"2026-04-22 02:39:37","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1761833,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-9128341/v1/ef6a50f2-c76e-4248-be7c-b572531cf0c2.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Two Pediatric Cases of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Predominantly Presenting as Cortical Encephalitis: A Case Report and Literature Review","fulltext":[{"header":"Introduction","content":"\u003cp\u003eMyelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is the most common type of idiopathic inflammatory demyelinating disorder of the central nervous system in children. The phenotypic spectrum of MOGAD is diverse, including optic neuritis, myelitis, acute disseminated encephalomyelitis, unifocal or multifocal cerebral lesions, brainstem or cerebellar involvement, and cerebral cortical encephalitis. Notably, cerebral cortical encephalitis represents a distinct phenotype of MOGAD (MOG-CCE), which is autoimmune-mediated and predominantly confined to the cerebral cortex \u003csup\u003e[1\u0026ndash;3]\u003c/sup\u003e.\u003c/p\u003e \u003cp\u003eThe pathogenesis of MOG-CCE remains to be fully elucidated. Current research suggests that MOG-CCE is an autoimmune disease mediated by anti-MOG antibodies, involving the participation of both humoral and cellular immunity. The proposed mechanism is as follows: First, environmental factors such as viral infections may trigger the activation and differentiation of MOG-specific CD4\u0026thinsp;+\u0026thinsp;T cells in peripheral lymphoid organs of genetically susceptible individuals \u003csup\u003e[4]\u003c/sup\u003e. Concurrently, B cells located in the periphery or within the central nervous system (CNS) may also become activated, differentiating into plasma cells and producing anti-MOG antibodies \u003csup\u003e[4, 5]\u003c/sup\u003e. These activated CD4\u0026thinsp;+\u0026thinsp;T cells, potentially synergizing with anti-MOG antibodies, then traverse the compromised blood-brain barrier (BBB) to enter the CNS parenchyma. Pathological studies \u003csup\u003e[5]\u003c/sup\u003e have provided supporting evidence for this hypothesis, revealing extensive inflammatory cell infiltration dominated by CD4\u0026thinsp;+\u0026thinsp;T cells (predominant) and CD20\u0026thinsp;+\u0026thinsp;B cells within the brain lesions of MOG-CCE, along with the phenomenon of macrophages engulfing MOG antigens (MOG-laden macrophages). These activated T cells further amplify the local inflammatory response through cytokine release. Concurrently, the anti-MOG antibodies that have entered the CNS exert their pathogenic effects through various pathways. Both the cortex and subcortical white matter can be involved, leading to clinical symptoms such as seizures and headache \u003csup\u003e[5]\u003c/sup\u003e. In summary, the pathogenesis of MOG-CCE is a multifactorial process resulting from the synergistic effects of specific T cell activation, antibody production, BBB disruption, and antibody effector functions. Within this process, CD4\u0026thinsp;+\u0026thinsp;T cell-driven cellular immunity likely plays an initial and central role, while antibodies primarily act as effector molecules.\u003c/p\u003e \u003cp\u003eSince the first report of unilateral cortical encephalitis with positive anti-MOG antibodies in 2017 \u003csup\u003e[6]\u003c/sup\u003e, pediatric MOGAD cases have remained rare. Herein, we report two pediatric cases of MOG antibody-positive CCE along with a review of the literature, aiming to enhance the understanding of this disease among pediatric clinicians.\u003c/p\u003e"},{"header":"Materials and methods","content":"\u003cp\u003eTo comprehensively delineate the clinical characteristics of MOG antibody-associated cerebral cortical encephalitis, we conducted a systematic literature search. The PubMed database was searched using the keywords \"Myelin Oligodendrocyte Glycoprotein\" and \"Cerebral Cortical Encephalitis.\" The Wanfang Database and China National Knowledge Infrastructure (CNKI) were searched using the keywords \"anti-myelin oligodendrocyte glycoprotein antibody\" and \"cortical encephalitis\". A cumulative total of 24 pediatric cases of MOG antibody-associated cortical encephalitis were retrieved from the literature [7–15]. Including the two cases reported herein, a total of 26 patients were analyzed. The inclusion criteria were: (1) age less than 18 years; (2) detection of serum anti-MOG antibodies at a titer greater than 1:10 at least once during the disease course; (3) cranial magnetic resonance imaging (MRI) revealing abnormal hyperintense signals predominantly confined to the cerebral cortex or sulci; and (4) an initial diagnosis of MOG-associated cortical encephalitis. The clinical characteristics, neuroimaging findings, and laboratory results of the 26 patients are summarized as follows (Table\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e\u003cdiv class=\"gridtable\"\u003e\u003cdiv align=\"left\" class=\"colspec\"\u003e\u003c/div\u003e\u003cdiv align=\"char\" class=\"colspec\"\u003e\u003c/div\u003e\u003cdiv align=\"left\" class=\"colspec\"\u003e\u003c/div\u003e\u003cdiv align=\"char\" class=\"colspec\"\u003e\u003c/div\u003e\u003ctable id=\"Tab1\" border=\"1\"\u003e \u003ccaption\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eSummary of clinical characteristics in 26 pediatric cases of MOG antibody-associated cortical encephalitis\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"4\"\u003e \u003c/colgroup\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\"\u003e \u003cp\u003eBasic clinical features\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\"\u003e \u003cp\u003en(%)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\"\u003e \u003cp\u003eLaboratory Findings, Treatment, and Outcomes\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\"\u003e \u003cp\u003en(%)\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003ctr\u003e \u003cth align=\"left\"\u003e \u003cp\u003eSex\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\"\u003e\u0026nbsp;\u003c/th\u003e \u003cth align=\"left\"\u003e \u003cp\u003eMOG\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\"\u003e\u0026nbsp;\u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eMale\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e12(46.15)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eNegative\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e0(0.00)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eFemale\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e14(53.84)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e \u003cp\u003ePositive\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e26(100.00)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003e\u003cb\u003eAge\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eCombined anti-NMDAR positivity[14, 15]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e4(15.38)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003ePreschool age(≤ 6)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e2(7.69)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e \u003cp\u003e\u003cb\u003eBrain MRI\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eSchool age(\u0026gt; 6)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e24(92.31)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eUnilateral cortical involvement\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e20(76.92)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003e\u003cb\u003eClinical Manifestations\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eBilateral cortical involvement\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e6(23.08)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eSeizures\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e19(73.08)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e \u003cp\u003e\u003cb\u003eTreatment\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eTodd's paresis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e5(19.23)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eMethylprednisolone pulse therapy\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e24(92.31)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eStatus epilepticus\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e9(34.62)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eIntravenous immunoglobulin\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e18(69.23)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eFever\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e13(50.00)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eImmunosuppressants\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e6(23.08)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eHeadache\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e14(53.84)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e \u003cp\u003e\u003cb\u003eOutcomes\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003ePsychiatric symptoms\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e6(23.08)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eRelapse\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e9(34.62)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eSpeech impairment\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e8(30.77)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eSequelae\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e7(26.92)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eVisual disturbances\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e8(30.77)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eDeath\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e0(0.00)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\"\u003e \u003cp\u003eParalysis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\"\u003e \u003cp\u003e11(42.31)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/table\u003e\u003c/div\u003e \u003cp\u003e\u003c/p\u003e \u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003cdiv id=\"Sec4\" class=\"Section3\"\u003e \u003c/div\u003e \u003c/div\u003e"},{"header":"Clinical data","content":"\u003ch2\u003ePatient 1:\u003c/h2\u003e\u003cp\u003eThe patient was a female infant, born in June 2013 via full-term vaginal delivery (G1P1), with a birth weight of 3300 g. There was no history of neonatal asphyxia, and the Apgar scores were 10 at both 5 and 10 minutes. Her family history was unremarkable.\u003c/p\u003e\u003cp\u003eInitial Presentation: At the age of 10 years and 9 months(on March 3, 2024), the patient was admitted to the Pediatric Intensive Care Unit (PICU) of Wuxi Children's Hospital due to \"recurrent convulsions for over 1 hour, accompanied by fever and vomiting.\" Her body weight at admission was 39 kg. During her PICU stay(6 days), she received intravenous immunoglobulin (IVIG) at a dose of 20 g/day for 2 days, intravenous methylprednisolone sodium succinate for anti-inflammatory therapy (2 mg/kg/day every 12 hours), and anti-seizure treatment with midazolam, propofol, and levetiracetam. After clinical improvement six days later, she was transferred to the Neurology Department for further management. Electroencephalography (EEG) performed during hospitalization revealed slow background activity (Fig.\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e). Cerebrospinal fluid (CSF) analysis upon admission showed a white blood cell count of 101 × 10⁶/L; a repeat CSF analysis 11 days later revealed a normalized white blood cell count of 6 × 10⁶/L. CSF biochemistry was normal on both occasions. Two cranial magnetic resonance imaging (MRI) scans (eight days apart) showed no significant abnormalities. She was discharged with a diagnosis of severe viral encephalitis. Upon discharge on March 15, she was prescribed oral levetiracetam (0.5 g twice daily), which was discontinued by her parents after one month, and a sequential course of oral prednisone for one month. A follow-up outpatient EEG two weeks later was normal.\u003c/p\u003e\u003cp\u003eFirst Relapse: Two months later, the patient presented to the outpatient clinic of Wuxi Children's Hospital with \"two episodes of vomiting accompanied by dizziness within one month.\" An electroencephalogram (EEG) on May 2 again revealed slow waves (Fig.\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e2\u003c/span\u003e). A follow-up cranial magnetic resonance imaging (MRI) scan on May 8 suggested \"right temporal gyral swelling with abnormal signals\" (Fig.\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e3\u003c/span\u003e), and hospital admission was scheduled accordingly. On May 11, the patient experienced a seizure episode while awake, characterized by generalized seizures lasting for over one hour, accompanied by a low-grade fever (peak 37.8°C). On the same day, she was brought by her parents to another hospital and admitted for treatment. During hospitalization, cerebrospinal fluid (CSF) analysis on May 12 revealed a white blood cell count of 36 × 10⁶/L, with normal CSF biochemistry. Serum testing for anti-MOG-IgG, anti-AQP4-IgG, and anti-GFAP-IgG was negative; however, CSF analysis was positive for anti-MOG-IgG at a titer of 1:1, while other antibodies were negative. The patient remained generally well during the first five days of hospitalization. On the afternoon of May 16, she experienced another seizure episode, characterized by focal seizures with left limb twitching. Therefore, a contrast-enhanced cranial MRI was performed on May 20, which revealed abnormal signals in the right temporal and frontal lobes. Contrast-enhanced MRI of the full spine and orbits showed no significant abnormalities. The diagnoses at that time were: 1. Central nervous system demyelinating disease (suspected MOGAD); 2. Convulsive status epilepticus. Treatment was initiated with intravenous methylprednisolone (900 mg/day for 3 days, followed by 450 mg/day for 3 days; body weight at that time was 45 kg) and oral levetiracetam (0.5 g twice daily) for seizure control. Upon discharge, the patient was continued on a sequential course of oral prednisone with monthly outpatient follow-up. A follow-up contrast-enhanced cranial MRI on October 15 showed \"significant improvement in the right temporal gyral swelling and abnormal signals compared to previous imaging\" (Fig.\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e4\u003c/span\u003e). Consequently, prednisone was tapered and discontinued after a total treatment duration of six months.\u003c/p\u003e\u003cp\u003eSecond Relapse: Four months after discontinuing prednisone, the patient was admitted to Wuxi Children's Hospital due to transient right limb twitching lasting half an hour, which occurred following an episode of anger. During this hospitalization, repeat cerebrospinal fluid (CSF) analysis and electroencephalography (EEG) were both normal. Cranial magnetic resonance imaging (MRI) performed on March 3, 2025, revealed \"abnormal signals in the right frontal and temporal lobes,\" involving the same regions as observed in May 2024 (Fig.\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e5\u003c/span\u003e). A live cell-based assay (CBA) revealed a serum anti-MOG-IgG antibody titer of 1:10+. The patient was treated with intravenous immunoglobulin (IVIG) pulse therapy (400 mg/kg/day for 5 days) and methylprednisolone pulse therapy (20 mg/kg/day for 3 days), followed by oral mycophenolate mofetil (0.5 g twice daily). At the one-year follow-up, the patient has remained relapse-free to date.\u003c/p\u003e\u003ch3\u003ePatient 2:\u003c/h3\u003e\u003cp\u003eThe patient was a female infant, born in July 2012 via full-term vaginal delivery (G2P2), with a birth weight of 3000 g. There was no history of neonatal asphyxia, and the Apgar scores were 10 at both 5 and 10 minutes. She has one healthy older brother, and her family history was unremarkable.\u003c/p\u003e\u003cp\u003eFrom March 5 to March 14, 2025, the patient experienced two episodes of afebrile seizures characterized by rightward deviation of both eyes and bilateral twitching of the left upper limb, lasting 3 minutes and 1 minute respectively before spontaneously resolving. On March 12, she experienced a transient episode of sudden loss of sensation in the left upper limb lasting over ten minutes, followed by residual numbness in the left upper limb upon recovery, which resolved spontaneously after approximately one hour. The patient was subsequently admitted to a local hospital. During hospitalization, she developed a low-grade fever (peak approximately 38°C) and received anti-infective and corticosteroid therapy, after which the fever subsided and she was discharged. However, she continued to experience recurrent dizziness and low-grade fever following discharge. Starting March 25, she developed headache and vomiting. On April 1, she was admitted to the Department of Neurology at Wuxi Children's Hospital due to \"recurrent low-grade fever for one month accompanied by convulsions, dizziness, and headache for one week.\" Cerebrospinal fluid (CSF) analysis performed upon admission (April 1) revealed a white blood cell count of 130 × 10⁶/L with normal CSF biochemistry. Serum testing for anti-MOG-IgG antibodies was positive at a titer of 1:100+, and CSF testing was positive at a titer of 1:10+. Cranial magnetic resonance imaging (MRI) performed on April 3 revealed abnormal signal intensity in the right frontal cortex (Fig.\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e6\u003c/span\u003e). Following admission, the patient received intravenous immunoglobulin (IVIG) pulse therapy (400 mg/kg/day for 5 days) and two courses of methylprednisolone pulse therapy (20 mg/kg/day for 3 days per course), with oral prednisone 60 mg daily for 4 days (body weight 52 kg) administered between the two pulse courses. Following clinical improvement, the patient was discharged on a sequential course of oral prednisone. During outpatient follow-up from June to August, she occasionally experienced transient visual phenomena described as hexagonal shapes, lasting several seconds and resolving spontaneously. At the one-year follow-up, she has remained relapse-free to date.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThis paper reports two cases of pediatric patients with MOG antibody-associated cerebral cortical encephalitis (MOG-CCE), which illustrate the typical clinical features of this condition in the pediatric population while also demonstrating clinical heterogeneity. Both patients presented with acute or subacute onset, with fever, seizures, and headache as the core symptoms [1, 16]. Brain magnetic resonance imaging (MRI) revealed characteristic focal cortical abnormalities on FLAIR sequences accompanied by swelling (localized in the right frontal-temporal lobe in patient 1 and the right frontal lobe in patient 2), consistent with previously described imaging features of MOG-CCE [1, 3, 17]. Diagnosis was confirmed in both cases by the presence of positive serum anti-MOG-IgG antibodies [2, 18], and both patients showed favorable responses to first-line immunotherapy (high-dose corticosteroids combined with intravenous immunoglobulin). However, notable differences were observed between the two cases. Patient 1 predominantly manifested with seizures and status epilepticus, whereas patient 2 presented with seizures, limb numbness, and recurrent low-grade fever. Although patient 2 exhibited higher anti-MOG-IgG antibody titers, no relapses occurred; conversely, patient 1 experienced recurrent episodes despite lower antibody titers. Based on these observations, we hypothesize that there is no significant correlation between anti-MOG-IgG antibody titers and the risk of relapse. However, previous studies have suggested that school-aged children with initial antibody titers exceeding 1:1280 (median age 10 years) have the highest probability of relapse within two years [19].\u003c/p\u003e \u003cp\u003eBased on the two cases reported in this study and a review of the literature, we summarized the clinical characteristics of 26 pediatric patients (aged\u0026thinsp;\u0026lt;\u0026thinsp;18 years) with MOG-CCE. The following findings were observed. Regarding demographic features, this condition predominantly affects school-aged and older children, with 92.31% of patients being over 6 years of age. The male-to-female ratio was approximately equal. This age distribution differs from that of adult MOG-CCE, which, according to current literature, can occur across all age groups, ranging from young adults to the middle-aged and elderly [1, 4].Clinically, seizures were the most prominent and core symptom, occurring in 73.08% of the 26 patients, with nearly half of these (9/19) presenting with status epilepticus. The incidence of seizures was considerably higher than that of other symptoms (headache 53.84%, fever 50%), indicating a tendency toward severe manifestations during the acute phase of this condition. For school-aged children with new-onset seizures, MOGAD should be included in the primary differential diagnosis [1, 16, 22]. Among the 26 patients, 4 cases (15.38%) were positive for concomitant anti-NMDAR antibodies. One of these cases [14] did not exhibit typical clinical symptoms and imaging features of anti-NMDAR encephalitis [20, 21], while the remaining 3 cases presented with mild anti-NMDAR encephalitis symptoms, consistent with previous reports [22]. Regarding imaging characteristics, the majority of patients (76.92%) exhibited unilateral cerebral cortical involvement on neuroimaging, which is highly consistent with imaging findings reported in adult patients [3, 17]. This observation suggests that anti-MOG antibody testing should be performed promptly when a patient presents with unilateral cortical encephalitis.In terms of treatment, the majority of patients showed a favorable response to first-line immunotherapy during the acute phase (methylprednisolone pulse therapy 92.31%, IVIG 69.23%). However, the relapse rate was relatively high, reaching 34.62%, with 23.08% of patients requiring long-term immunosuppressive agents to control relapses. The two most commonly used immunosuppressants were rituximab and mycophenolate mofetil. Regarding prognosis, some patients experienced a relapsing disease course [23]; however, no fatalities occurred among the 26 MOG-CCE cases. Most patients achieved complete recovery, indicating a generally favorable prognosis. Sequelae were observed in 26.92% (7 cases) of patients, including two patients who regained most functions with only mild articulation difficulties [7, 10], two patients with mild visual disturbances [15], and three patients who developed recurrent secondary epilepsy [11, 12] along with cognitive impairment and motor function deficits [11]. Overall, the prognosis in this pediatric cohort was better than that reported in adult cases.\u003c/p\u003e \u003cp\u003ePediatric MOGAD is an autoimmune disorder predominantly affecting school-aged children, with acute seizures (often presenting as status epilepticus) as its core clinical manifestation and unilateral cortical involvement as a characteristic imaging feature. Diagnosis relies on the detection of specific anti-MOG antibodies, with the cell-based assay (CBA) being the recommended method. While patients generally respond well to immunosuppressive therapy during the acute phase, the condition carries a significant risk of relapse. A subset of patients requires long-term immunosuppressive treatment and may experience residual sequelae. Pediatric neurologists should enhance their awareness of this entity to facilitate early diagnosis and implement individualized long-term management strategies .\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eAcknowledgments\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWe would like to express our gratitude to the patients and their parents for providing the case data.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll authors meet the ICMJE authorship criteria.YH,JM designed the study. LZ, XH collected and analyzed the data. JM,LF drafted the manuscript. SL provided imaging images. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConflict of interest\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthics statement\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe studies involving humans were approved by Ethics board approval and consent was obtained for this work from the Ethics Committee at the Children\u0026rsquo;s Hospital of Jiangnan University,Wuxi, Jiangsu, China (Ethics Number: WXCH2025-11-173).\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWritten informed consent for publication of the clinical details and clinical images was obtained from the the patient\u0026rsquo;s parent. A copy of the consent form is available for review by the Editor of this journal.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n \u003cli\u003eShu H, Ding M, Shang P, Song J, Lang Y, Cui L. Myelin Oligodendrocyte Glycoprotein Antibody Associated Cerebral Cortical Encephalitis: Case Reports and Review of Literature. Front Hum Neurosci. 2022 Jan 3;15:782490.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eFujimori J. [Anti-myelin oligodendrocyte glycoprotein antibody associated encephalitis]. Rinsho Shinkeigaku. 2020 Feb 27;60(2):117-119. Japanese.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eGuo L, Yun HJ, Tan X, Geng X, Ding Y. A case of unilateral recurrent cerebral cortical encephalitis with anti-myelin oligodendrocyte glycoprotein antibodies. Brain Circ. 2022 Jun 30;8(2):102-107.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eOgawa R, Nakashima I, Takahashi T, Kaneko K, Akaishi T, Takai Y, Sato DK, Nishiyama S, Misu T, Kuroda H, Aoki M, Fujihara K. MOG antibody-positive, benign, unilateral, cerebral cortical encephalitis with epilepsy. Neurol Neuroimmunol Neuroinflamm. 2017 Jan 16;4(2):e322.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eHamid SHM, Whittam D, Saviour M, Alorainy A, Mutch K, Linaker S, Solomon T, Bhojak M, Woodhall M, Waters P, Appleton R, Duddy M, Jacob A. Seizures and Encephalitis in Myelin Oligodendrocyte Glycoprotein IgG Disease vs Aquaporin 4 IgG Disease. JAMA Neurol. 2018 Jan 1;75(1):65-71.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eRuss JB, Timbie CM, Li Y, Gonzalez-Giraldo E. Clinical Reasoning: An 11-year-old girl with focal seizures, fevers, and unilateral, enhancing cortical lesions. Neurology. 2020 Dec 8;95(23):e3153-e3159. \u003c/li\u003e\n \u003cli\u003eTian F, Liu X, Yang C, Wang B, Song Z, Zhang Y. MOG antibody-positive cerebral cortical encephalitis: Two case reports and literature review. Int J Dev Neurosci. 2021 Jun;81(4):342-351.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eAhsan N, Jafarpour S, Santoro JD. Myelin oligodendrocyte glycoprotein antibody encephalitis following severe acute respiratory syndrome coronavirus 2 in a pediatric patient. Clin Exp Pediatr. 2021 Jun;64(6):310-312.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eDoig D, McNamara C, Mewasingh L, Beri S, Jones B, Kachramanoglou C, Jan W. Autoimmune cortical encephalitis in two children with anti-myelin oligodendrocyte glycoprotein (MOG) antibody. J Neurol. 2021 Mar;268(3):1096-1101.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eTakamatsu T, Yamanaka G, Uryu H, Takeshita M, Morishita N, Morichi S, Ishida Y, Oana S, Terashi H, Shichino H, Sakuma H, Kawashima H. Improvement in recurrent anti-myelin oligodendrocyte glycoprotein antibody - positive cerebral cortical encephalitis not requiring anti - inflammatory therapy following the decrease in cytokine/chemokine levels. Mult Scler Relat Disord. 2020 Aug;43:102168.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003ePeng M, Qu Z, Zhang Y, et al. A case report and literature review of anti-MOG antibody-positive childhood cortical encephalitis. J Clin Pediatr. 2021;39(8):588-591. (Chinese)\u003c/li\u003e\n \u003cli\u003eZhou J, Ding C, Zhang W, et al. Clinical characteristics of anti-myelin oligodendrocyte glycoprotein antibody-associated disease presenting as cortical encephalitis in children.\u0026nbsp;Natl Med J China. 2020;100(25):1952-1955. (Chinese)\u003c/li\u003e\n \u003cli\u003eChen Y, Yang Z, Zhou H, et al. Clinical characteristics analysis of patients with MOG antibody-associated cortical encephalitis.\u0026nbsp;J Epilepsy Neuroelectrophysiol. 2024;33(5):284-292, inside back cover, back cover. (Chinese)\u003c/li\u003e\n \u003cli\u003eOtani T, Irioka T, Igarashi S, Kaneko K, Takahashi T, Yokota T. Self-remitting cerebral cortical encephalitis associated with myelin oligodendrocyte glycoprotein antibody mimicking acute viral encephalitis: A case report. Mult Scler Relat Disord. 2020 Jun;41:102033.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eAn JY, Jang SI, Choi SG, Lee SN, Lee EJ, Kim KK, Kim HR. Myelin oligodendrocyte glycoprotein antibody-associated disease presenting as unilateral cerebral cortical encephalitis: a case report. Encephalitis. 2024 Apr;4(2):35-39.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eLiu M, Li D. Myelin oligodendrocyte glycoprotein antibody-associated cerebral cortical encephalitis: a case report highlighting diagnostic challenges and therapeutic implications. Front Immunol. 2025 Jun 18;16:1619807.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eHennes EM, Baumann M, Schanda K, Anlar B, Bajer-Kornek B, Blaschek A, Brantner-Inthaler S, Diepold K, Eisenk\u0026ouml;lbl A, Gotwald T, Kuchukhidze G, Gruber-Sedlmayr U, H\u0026auml;usler M, H\u0026ouml;ftberger R, Karenfort M, Klein A, Koch J, Kraus V, Lechner C, Leiz S, Leypoldt F, Mader S, Marquard K, Poggenburg I, Pohl D, Pritsch M, Raucherzauner M, Schimmel M, Thiels C, Tibussek D, Vieker S, Zeches C, Berger T, Reindl M, Rost\u0026aacute;sy K; BIOMARKER Study Group. Prognostic relevance of MOG antibodies in children with an acquired demyelinating syndrome. Neurology. 2017 Aug 29;89(9):900-908.\u003c/li\u003e\n \u003cli\u003eZhou L, ZhangBao J, Li H, Li X, Huang Y, Wang M, Zhao C, Lu J, Lu C, Li Y, Quan C. Cerebral cortical encephalitis followed by recurrent CNS demyelination in a patient with concomitant anti-MOG and anti-NMDA receptor antibodies. Mult Scler Relat Disord. 2017 Nov;18:90-92.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eChinese Society of Neurology. Chinese expert consensus on diagnosis and treatment of autoimmune encephalitis.Chin J Neurol. 2017;50(2):91-98. (Chinese)\u003c/li\u003e\n \u003cli\u003eKunchok A, Flanagan EP, Krecke KN, Chen JJ, Caceres JA, Dominick J, Ferguson I, Kinkel R, Probasco JC, Ruvalcaba M, Santoro JD, Sieloff K, Timothy J, Weinshenker BG, McKeon A, Pittock SJ. MOG-IgG1 and co-existence of neuronal autoantibodies. Mult Scler. 2021 Jul;27(8):1175-1186.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eXiang XM, Evans R, Lovera J, Rao R. Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Presenting as Recurrent and Migrating Focal Cortical Encephalitis. Child Neurol Open. 2020 Nov 15;7:2329048X20966172.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eCorbali O, Chitnis T. Pathophysiology of myelin oligodendrocyte glycoprotein antibody disease. Front Neurol. 2023 Feb 28;14:1137998.\u0026nbsp;\u003c/li\u003e\n \u003cli\u003eTakai Y, Misu T, Kaneko K, Chihara N, Narikawa K, Tsuchida S, Nishida H, Komori T, Seki M, Komatsu T, Nakamagoe K, Ikeda T, Yoshida M, Takahashi T, Ono H, Nishiyama S, Kuroda H, Nakashima I, Suzuki H, Bradl M, Lassmann H, Fujihara K, Aoki M; Japan MOG-antibody Disease Consortium. Myelin oligodendrocyte glycoprotein antibody-associated disease: an immunopathological study. Brain. 2020 May 1;143(5):1431-1446. \u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-neurology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"nurl","sideBox":"Learn more about [BMC Neurology](http://bmcneurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/nurl","title":"BMC Neurology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Cortical encephalitis, Pediatric myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), Live cell-based assay (CBA)","lastPublishedDoi":"10.21203/rs.3.rs-9128341/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-9128341/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eObjective\u003c/h2\u003e \u003cp\u003eTo analyze and summarize the clinical characteristics of pediatric patients with myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) presenting with cortical encephalitis as the predominant clinical phenotype, thereby enhancing clinical awareness and facilitating early diagnosis and treatment.\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e \u003cp\u003eWe retrospectively analyzed the clinical data of two pediatric MOGAD cases with a predominant cortical encephalitis phenotype admitted to Wuxi Children's Hospital from March 2024 to March 2025. Their clinical presentations, treatments, and prognoses were summarized alongside a relevant literature review.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e \u003cp\u003eIn Patient 1, the patient initially presented with convulsive status epilepticus (March 2024) and normal cranial MRI, diagnosed as \"severe encephalitis.\" After initial improvement, follow-up MRI two months later revealed frontotemporal cortical swelling, followed by another episode of status epilepticus one week subsequently. At that time, CSF was positive for MOG-IgG (titer 1:1), but serum was negative. The patient improved with immunotherapy. In March of this year, despite being asymptomatic, routine MRI again showed frontotemporal cortical swelling, and serum MOG-IgG was positive (titer 1:10+; live CBA). Acute treatment included IVIG and pulsed steroids, and the patient is now maintained on corticosteroids and mycophenolate mofetil. Patient 2 presented with prolonged fever,convulsions, headache, vomiting, and limb numbness. Serum MOG-IgG titer was 1:100+ (CBA), and MRI showed diffuse cerebral cortical swelling. The patient improved following IVIG and pulsed steroid therapy. Neither patient had relapsed at the one-year follow-up.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003ePediatric myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) can manifest as cortical encephalitis, typically presenting with core symptoms including fever, headache, and seizures. The cortical encephalitis phenotype of MOGAD is more commonly observed in older children. Patients generally respond well to acute-phase treatment with intravenous immunoglobulin (IVIG) and pulsed methylprednisolone; however, a subset may experience relapses, necessitating timely initiation of second-line immunosuppressive therapy. When neuroimaging reveals features suggestive of cortical encephalitis, MOG antibody testing should be performed to confirm the diagnosis, preferably using a live cell-based assay (CBA) which offers higher sensitivity.\u003c/p\u003e","manuscriptTitle":"Two Pediatric Cases of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Predominantly Presenting as Cortical Encephalitis: A Case Report and Literature Review","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-04-19 11:59:17","doi":"10.21203/rs.3.rs-9128341/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"editorInvitedReview","content":"","date":"2026-04-21T16:10:28+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"105678913095989423606971263597258953148","date":"2026-04-16T01:15:22+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-04-09T04:42:14+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2026-03-25T12:28:47+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-03-25T07:24:43+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-03-25T07:24:23+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Neurology","date":"2026-03-15T11:47:57+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-neurology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"nurl","sideBox":"Learn more about [BMC Neurology](http://bmcneurol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/nurl","title":"BMC Neurology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"388989b5-53f7-4b06-a040-9f5172bbc265","owner":[],"postedDate":"April 19th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-04-19T11:59:17+00:00","versionOfRecord":[],"versionCreatedAt":"2026-04-19 11:59:17","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-9128341","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-9128341","identity":"rs-9128341","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}