Clinical Characteristics and Short-Term Outcomes of Pediatric Autoimmune Encephalitis: A Single-Center Cohort Study

Clinical Characteristics and Short-Term Outcomes of Pediatric Autoimmune Encephalitis: A Single-Center Cohort Study | 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 Research Article Clinical Characteristics and Short-Term Outcomes of Pediatric Autoimmune Encephalitis: A Single-Center Cohort Study Thi Nguyet Dao, Thanh Huong Do, Thi Bich Van Nguyen, Vu Hung Cao, and 2 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8062052/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 13 You are reading this latest preprint version Abstract Objective The study aimed to investigate the clinical characteristics and short-term outcomes of children with autoimmune encephalitis (AE) in North Vietnam. Methods We conducted a prospective cohort study of 102 children diagnosed with AE at the Vietnam National Children’s Hospital between August 2023 and September 2025 based on Cellucci et al. criteria 2020. Demographic, clinical, laboratory, neuroimaging, and antibody data were collected. Short-term (3-month) outcomes were assessed using the modified Rankin Scale (mRS) by the pediatric neurologist. The children were divided into good (scores ≤ 2) and poor (scores > 2). Results The mean age was 8.4 ± 3.9 years, with a male-to-female ratio of 1:1.5. Anti-NMDAR AE accounted for 80% of antibody-positive cases, followed by anti-MOG (18.7%) and anti-GABA (1.3%). The most common symptoms were speech disorders (85.3%), sleep disorders (76.5%), seizures (57.8%), and behavioral abnormalities (53.9%). At 3 months, 74.5% achieved good recovery (mRS ≤ 2), with higher rates in anti-MOG (78.6%) and antibody-negative (85.2%) groups, and the lowest in anti-NMDAR AE (68.3%). Independent predictors of poor outcome included dyskinesia (OR 3.39, p = 0.049), higher maximum mRS (OR 2.66, p = 0.019), and longer hospitalization (OR 1.05 per day, p = 0.024). Conclusion Pediatric AE shows heterogeneous presentations, predominantly anti-NMDAR AE, which tends to be more severe. Early recognition of prognostic indicators may improve treatment strategies. autoimmune encephalitis clinical features short-term outcomes pediatric Figures Figure 1 Figure 2 Introduction Autoimmune encephalitis (AE) is an immune-mediated inflammatory disorder of the brain parenchyma caused by autoantibodies targeting neuronal surface proteins, receptors, ion channels, or sometimes unidentified antigens [ 1 ]. Recent advances in immunological assays have led to the discovery of several specific autoantibodies, including those against myelin oligodendrocyte glycoprotein (MOG), N-methyl-D-aspartate receptor (NMDAR), leucine-rich glioma-inactivated 1 (LGI1), gamma aminobutyric acid-A (GABA), and contactin-associated protein-like 2 (CASPR2), among others [ 2 ]. Among these, anti-NMDAR encephalitis is the most common subtype in children, accounting for approximately 40% of AE cases. The clinical presentation of AE is heterogeneous, typically with an acute or subacute onset of seizures, cognitive dysfunction, altered consciousness, behavioral and emotional disturbances, and sleep disorders [ 3 ]. Several studies have demonstrated that distinct antibody subtypes are associated with characteristic clinical profiles, whereas a proportion of patients exhibit typical AE manifestations but remain seronegative [ 2 , 4 ]. This highlights the diagnostic challenge of recognizing AE and predicting antibody subtypes in pediatric patients based solely on clinical features. First-line immunotherapy includes high-dose corticosteroids, intravenous immunoglobulin (IVIg), or plasma exchange (PLEX). Patients who do not respond may require second-line agents such as rituximab or cyclophosphamide [ 5 ]. Prognosis varies depending on the antibody subtype. Most children with anti-NMDAR encephalitis have a favorable long-term outcome, although some may experience persistent sequelae such as refractory epilepsy, memory impairment, psychiatric disorders, or even death. Patients with LGI1 antibody-associated AE typically respond rapidly to immunotherapy but may have poorer long-term outcomes than those with NMDAR antibodies. In contrast, anti-MOG AE generally shows a good response to immunotherapy and favorable recovery at discharge [ 6 , 7 ]. In a study by Lee et al. (2021), 62.2% of 37 seronegative AE patients achieved good functional outcomes with modified Rankin Scale (mRS) 0–1 at one-year follow-up, although the relapse rate remained high (35.1%) [ 4 ]. In Vietnam, research on autoimmune encephalitis in children remains limited, and data on the clinical characteristics, antibody profiles, and short-term outcomes are scarce. Early recognition and timely initiation of immunotherapy are crucial for improving prognosis; however, the presentation in children is often atypical, leading to diagnostic and therapeutic delays. Therefore, this prospective study aimed to analyze the clinical manifestations, laboratory and neuroimaging findings, immunotherapy approaches, and short-term outcomes of children diagnosed with autoimmune encephalitis at the Vietnam National Children’s Hospital. The findings are expected to provide valuable reference data to support early diagnosis, optimize treatment strategies, and improve clinical management of autoimmune encephalitis in Vietnamese children. Methods Study design This prospective study included 102 children diagnosed with AE at the Neurology Department, Vietnam National Children’s Hospital, between August 2023 and September 2025. All patients met the diagnostic criteria for AE proposed by Cellucci et al. (2020): (1) acute or subacute onset (< 3 months) of neurological or psychiatric symptoms; (2) at least two signs of central nervous system dysfunction; (3) at least one paraclinical indicator of inflammation; and (4) reasonable exclusion of alternative causes [ 2 ]. Patients fulfilling the diagnostic criteria for acute disseminated encephalomyelitis (ADEM) or had only the clinical criteria, without supportive paraclinical evidence of inflammation and with negative antibody findings, were excluded from the study. Clinical Data Analysis Clinical information was obtained through direct interviews with caregivers and review of medical records, including demographic characteristics, clinical manifestations, magnetic resonance imaging (MRI) findings, electroencephalography (EEG) abnormalities, cerebrospinal fluid (CSF) parameters, tumor markers, treatment modalities, and outcomes. Each patient was examined at admission and re-evaluated at 3 months post-treatment. The mRS was used to assess neurological disability, ranging from 0 (no symptoms) to 6 (death) [ 8 ]. Scores were assigned by a pediatric neurologist at disease onset, at the time of peak severity, and at 3-month follow-up. An mRS ≤ 2 after 3 months was defined as a good short-term outcome, while an mRS > 2 indicated partial recovery. Patients achieving an mRS of 0 were considered to have complete recovery. Antibody testing Autoantibody assays were performed on serum or cerebrospinal fluid samples, using indirect immunofluorescence assays. Tested antibodies included NMDAR, GABABR, LGI1, CASPR2, AMPA1, AMPA2, and DPPX in serum or CSF, using the autoimmune encephalitis mosaic 6 kit; while anti-MOG antibodies were analyzed in serum, using NMOSD screen 1 EUROPattern aquaporin-4 and MOG (Euroimmun). Samples were processed at the Department of Molecular Biology for Infectious Diseases, Vietnam National Children’s Hospital. Statistical analysis Statistical analyses were performed using SPSS software version 20.0. Normally distributed continuous variables were presented as mean ± standard deviation and compared using the independent-samples t-test; whereas non-normally distributed variables were expressed as median and interquartile range and compared using the Mann-Whitney U test. Categorical variables were expressed as frequencies and percentages, and intergroup comparisons were made using the chi-square test or Fisher’s exact test, as appropriate. A p -value 2). Variables with p < 0.1 in univariate analysis were entered into the model. Results Demographic characteristics Among 102 children with autoimmune encephalitis, anti-NMDAR antibodies were detected in 58.8%, anti-MOG antibodies in 13.7%, and anti-GABA antibodies in 0.9%, while 26.5% of patients were antibody-negative. Among antibody-positive patients (n = 75), anti-NMDAR AE predominated (80%), followed by anti-MOG (18.7%) and anti-GABA (1.3%). The mean age at onset of AE was 8.4 ± 3.9 years, ranging from 1 to 16 years, with a male-to-female ratio of 1:1.5. The majority of patients (86.3%) were of Kinh ethnicity, with the remaining cases belonging to other ethnic groups such as Tay, Nung, Thai, Muong, and Dao. Demographic features of patients with different types of AE are summarized in Table 1. Clinical features of pediatric autoimmune encephalitis Among the 102 patients, the most common clinical manifestations were seizures, speech disorders, behavioral abnormalities, sleep disorders, and memory deficits. In the anti-NMDAR AE, the most common symptoms included speech disorders, behavioral and sleep disorders, dyskinesia, and hypertonia. Patients with anti-MOG AE more frequently presented with seizures, speech disorders, focal neurological signs, and impaired consciousness. Two patients were found to have ovarian teratomas, both of whom tested positive for anti-NMDAR antibodies. Clinical features of patients with different types of AE are summarized in Figure 1. Figure 1. Heatmap showing the frequency of clinical manifestations in autoimmune encephalitis according to antibody subtype AE: Autoimmune encephalitis; NMDA: N-methyl-D-aspartate; MOG: Myelin oligodendrocyte glycoprotein. Laboratory, cerebrospinal fluid, EEG, and neuroimaging findings All patients in the study underwent CSF analysis, EEG, and brain MRI or computed tomography (CT) at admission. Among 102 patients, 100 patients underwent brain MRI, and 2 patients underwent CT scans. Abnormal neuroimaging findings were detected in 40 patients (39.2%). When analyzed by antibody subtype, all patients with anti-MOG AE showed abnormal brain MRI (14/14, 100%), most commonly involving the cortical, subcortical, and deep gray matter regions (Figure 2). Abnormal MRI findings were observed in 25% of patients with anti-NMDA AE and in 40.7% of antibody-negative cases, although the lesions were generally nonspecific. Figure 2 . Brain MRI images on T2-FLAIR sequences of some patients with anti-MOG AE (A) Cortical and subcortical lesions in bilateral fronto-parietal lobes; (B) Bilateral putamen and thalamic lesions; (C) Bilateral cortical–subcortical lesions; (D) Bilateral caudate nuclei, putamen, internal and external capsule lesions; (E) Cortical and thalamic lesions; (F) Bilateral putamen and thalamic lesions. CSF examination was performed in all patients upon admission, revealing pleocytosis (> 5 cells/mm³) in 83.3% and elevated protein levels (> 0.45 g/L) in 10.8% of cases. EEG was conducted in all patients, with abnormalities detected in 75.5%. The most common findings were diffuse or focal background slowing (72.5%), while epileptiform discharges were present in 11.8% of patients. Typical imaging and EEG findings of patients included in the study are shown in Table 2. [Insert Table 2 here] Treatment and outcomes All patients in our study received first-line immunotherapy, including high-dose methylprednisolone (20 mg/kg/day for 5 days), IVIg (400 mg/kg/day for 5 days), and/or PLEX. Among them, 52% of patients were treated with methylprednisolone alone, 42.2% received a combination of methylprednisolone and IVIg, 1% were treated with IVIg and PLEX, and 4.9% received a combination of methylprednisolone, IVIg, and PLEX. Seventeen of the 102 patients received second-line therapy with rituximab, including 14 patients with anti-NMDAR AE and 2 with anti-MOG AE. Six patients (5.9%) required third-line immunotherapy using tocilizumab or bortezomib, all of whom belonged to the anti-NMDAR AE group. We used the mRS to assess the clinical efficacy at disease onset, peak stage, and 3-month follow-up treatment. The mean mRS score at onset was 2 (IQR: 1-2), and the median maximum mRS score was 3.5 (IQR: 2-5). At 3 months, 74.5% of patients achieved good recovery (mRS ≤ 2). The proportion of good recovery was higher in patients with the anti-MOG AE (78.6%) and the antibody-negative AE (85.2%). Treatment and outcomes of patients included in the study are shown in Table 3. [Insert Table 3 here] 74.5% of patients achieved good recovery after 3 months (mRS ≤ 2). When stratified by antibody subtype, the rates of good recovery at 3 months were significantly higher in patients with anti-MOG AE and antibody-negative AE than in those with anti-NMDAR AE (78.6% and 85.2% vs. 68.3%). Analysis of factors associated with poor recovery showed that patients presenting with altered consciousness at admission, behavioral abnormalities, dyskinesia, hypertonia, abnormal EEG background activity, longer hospital stay, and higher mRS scores at onset and peak stage had significantly lower rates of good recovery after 3 months ( p < 0.05) (Table 4). [Insert Table 4 here] Multivariate logistic regression analysis identified dyskinesia, higher maximum mRS score, and longer hospital stay as independent predictors of poor short-term outcome after 3 months ( p < 0.05) (Table 5). Discussion Our study included 102 pediatric patients diagnosed with AE. Among antibody-positive patients (n = 75), anti-NMDAR AE predominated (80%), followed by anti-MOG (18.7%) and anti-GABA (1.3%). These findings are consistent with previous reports. In this study, the most common clinical manifestations were seizures, speech disorders, behavioral abnormalities, dyskinesia, and sleep disorders. When stratified by antibody subtype, patients with anti-NMDAR AE exhibited higher frequencies of memory deficits, behavioral abnormalities, speech disorders, dyskinesia, and hypertonia compared with other groups. In contrast, patients with anti-MOG AE typically presented with seizures, altered consciousness, and focal neurological signs, while antibody-negative AE was more often associated with seizures, speech disorders, and sleep disorders. These findings align with observations from Cellucci et al., Lee et al., and Wegener-Panzer et al [2, 4, 7]. The clinical diversity among subtypes may be related to the specific target receptor and its functional role in neuronal signaling. The NMDAR plays a critical role in synaptic plasticity, learning, memory, and emotion regulation. Studies have shown that anti-NMDAR antibodies selectively bind to and induce internalization of surface NMDARs, leading to decreased glutamatergic synaptic transmission and resulting in neurological symptoms such as memory deficits and behavioral abnormalities [9]. The underlying triggers of AE in children remain unclear. Several studies suggest that anti-NMDAR AE can occur following viral infections or in association with ovarian or testicular tumors. Reported viral triggers include Herpes simplex virus (HSV), Japanese encephalitis virus (JEV), and coronaviruses [1]. In our cohort, five cases developed AE following viral infections (two patients following HSV infection, two cases following JEV infection, and one case following hand-foot-and-mouth disease). In addition, 21 patients reported preceding respiratory infections within two weeks before disease onset, supporting the hypothesis that viral infections may act as potential triggers for AE. Ovarian teratoma has been recognized as an important trigger for anti-NMDAR AE, particularly in older children and young women. Previous studies reported a prevalence ranging from 1.17% to 56%, higher among adolescents and adults [10]. Therefore, screening for ovarian or testicular tumors should be considered in all pediatric patients, especially in older girls. In our study, all patients underwent abdominal ultrasound or CT, and ovarian teratomas were detected in 2% of patients, both of whom were positive for anti-NMDAR antibodies. The lower frequency in our cohort may be attributed to the younger average age (mean 8.4 ± 3.9 years) compared with other studies. Analysis of brain MRI findings showed abnormalities in 39.2% of patients. Abnormalities were observed in 25% of patients with anti-NMDAR AE, 100% of those with anti-MOG AE, and 40.7% of antibody-negative patients. In the anti-NMDAR group, lesions were mostly nonspecific and involved cortical or subcortical regions (6.7%), brain parenchyma (6.7%), and deep gray matter (5%). In contrast, all patients in the anti-MOG AE group demonstrated abnormal MRI findings, most commonly affecting cortical-subcortical areas (50%), deep gray matter (62.3%), brain parenchyma (35.7%), and the cerebellum (28.6%). MOG is a myelin protein located on the outer surface of the myelin sheath, distributed primarily in the white matter of the brain, spinal cord, and optic nerves. Previous studies have reported anti-MOG antibodies in acute disseminated encephalomyelitis, optic neuritis, and transverse myelitis. However, recent reports have described anti-MOG AE as an emerging clinical phenotype in children. A study from China in 2022 reported 18 pediatric patients with anti-MOG AE but without demyelinating lesions on MRI. That study noted that the most common symptoms were altered consciousness, prolonged fever, headache, seizures, and focal neurological deficits, with MRI showing T2-hyperintense lesions in the cortex, basal ganglia, thalamus, cerebellum, and brainstem [11]. Our findings are consistent with these observations, further supporting that anti-MOG AE represents a distinct clinical entity within the AE spectrum. Testing for anti-MOG antibodies should be considered in children presenting with acute neurological dysfunction and MRI abnormalities suggestive of inflammatory involvement. All patients underwent an EEG at admission. Abnormal EEG findings were observed in 73.5% of cases, most commonly diffuse background slowing, while epileptiform discharges were detected in 11.8%. There were no significant differences in EEG patterns among antibody subtypes. These results are consistent with those of Jha et al. (2024), who reported background slowing in approximately 82% and epileptiform activity in 25.6% of patients [12].In several cases, children presented with subtle neuropsychiatric symptoms but exhibited abnormal EEG background activity, suggesting that EEG may serve as a sensitive tool for early detection of AE in pediatric patients. All patients in our study received first-line immunotherapy, including steroids, IVIg, and/or PLEX. Of these, 52% were treated with steroids alone, 47.1% received combination therapy with IVIg, and 5.9% underwent PLEX. Seventeen patients (16.7%) required second-line immunotherapy with rituximab (375 mg/m² weekly for 4 weeks), while 6 patients (5.9%) required third-line therapy (2 received bortezomib and 4 received tocilizumab). Among those receiving second-line treatment, 14 (82.4%) had anti-NMDAR AE, 2 (11.8%) had anti-MOG AE, and 1 (5.9%) had anti-GABA receptor AE. All patients requiring third-line therapy were anti-NMDAR positive, indicating that this subtype tends to have more severe disease and slower recovery. In our study, one patient was diagnosed with anti-GABA AE. The patient initially presented with memory deficits and behavioral abnormalities, but was diagnosed six months after symptom onset. Despite receiving immunotherapy (steroids and rituximab), the clinical improvement was only about 50% after three months of treatment. This case highlights that delayed diagnosis and initiation of therapy may result in suboptimal recovery outcomes. At 3-month follow-up, the rate of good recovery (mRS ≤ 2) was lowest in the anti-NMDAR AE (68.3%), while higher recovery rates were observed in the anti-MOG AE (78.6%) and antibody-negative AE (85.2%). These findings are consistent with those reported by Lee et al. and Wegener-Panzer et al [4, 7]. Their results observed better early recovery in anti-MOG AE and antibody-negative AE, while anti-NMDAR AE often required longer recovery periods, possibly due to delayed receptor functional restoration. Several studies have shown that complete recovery from anti-NMDAR AE may take up to two years [1, 2]. Several clinical features, such as altered consciousness, behavioral abnormalities, and dyskinesia, were associated with a significantly higher risk of incomplete recovery compared with those without these symptoms. These findings are consistent with Kang et al. (2022), who reported that intensive care unit admission, high peak mRS scores, status epilepticus, and HSV-associated onset were predictive of poorer outcomes [13]. This suggests that severe neurological dysfunction at onset is an important indicator of poor prognosis. Biological factors also contribute to determining outcomes. Elevated lymphocyte counts in CSF and slowing in EEG background activity indicate ongoing neuroinflammation and the degree of cortical involvement. Additionally, concurrent infections were strongly linked to unfavorable outcomes, likely by worsening the inflammatory response and extending the duration of treatment. In our cohort, longer hospital stays and higher maximum mRS scores were significantly associated with partial recovery. This suggests that the initial severity of the disease and treatment-related complications have a considerable impact on functional outcomes. On the other hand, factors such as age, sex, and MRI abnormalities showed no significant correlation in univariate analysis. Multivariate logistic regression analysis identified dyskinesia, higher maximum mRS score, and longer hospital stay as independent predictors of poor short-term recovery. Patients with dyskinesia were approximately 3.4 times more likely to have poor recovery. Similarly, higher maximum mRS scores were strongly correlated with worse outcomes, reflecting the influence of initial disease severity on prognosis. Prolonged hospital stay also predicted unfavorable outcomes, suggesting that severe or complicated cases require longer treatment and have a lower likelihood of full recovery. Previous studies have shown that early initiation of therapy and the use of combination immunotherapy can lead to complete recovery without relapse [5, 6]. In our study, the rate of good recovery at 3 months was 74.3%, which is higher than the 48.2% reported by Raza M. (2024) [14]. This difference may be explained by the fact that our patients presented with milder symptoms, with a median mRS score at onset of 2 (IQR: 1 - 2) and a maximum mRS score of 3.5 (IQR: 2 - 5), whereas in Raza’s study, the median mRS score at onset was 5 (IQR: 4 - 5). However, follow-up beyond 6–12 months is necessary, as delayed neurological recovery and relapses are frequent in AE, particularly in anti-NMDAR cases. This study is limited by its single-center design, relatively short follow-up, and lack of quantitative MRI or antibody titration data, which may underestimate long-term sequelae. Conclusion Pediatric autoimmune encephalitis in Vietnam predominantly involves anti-NMDAR antibodies and presents with diverse neurological symptoms. Most children respond well to first-line immunotherapy, yet dyskinesia, higher maximum mRS, and prolonged hospitalization predict poorer short-term recovery. Early identification and aggressive management of these risk factors may improve outcomes. Abbreviations AE Autoimmune encephalitis mRS modified Rankin Scale MOG Myelin oligodendrocyte glycoprotein NMDAR N-methyl-D-aspartate receptor GABA Gamma aminobutyric acid-A LGI1 Leucine-rich glioma-inactivated 1 CASPR2 Contactin-associated protein-like 2 IVIg Intravenous immunoglobulin PLEX Plasma exchange MRI Magnetic resonance imaging CT Computed Tomography EEG Electroencephalography CSF Cerebrospinal fluid JEV Japanese encephalitis virus HSV Herpes simplex virus HFMD Hand, Foot, and Mouth Disease OR Odds Ratio IQR Interquartile range CT Computed Tomography SD Standard Deviation Declarations Acknowledgment The authors thank the clinicians and nurses at the Department of Neurology and Molecular Biology for Infectious Disease, Vietnam National Children’s Hospital, for their dedicated support in patient management and data collection. Author Contributions Thi Nguyet Dao and Thanh Huong Do: Design, Writing – review & editing, Data collection, Analysis, and Interpretation. Thi Bich Thuy Phung: Design, Methodology, Writing – review & editing, Supervision. Thi Bich Van Nguyen, Thi Van Nguyen, and Vu Hung Cao: Data collection, Analysis. Funding This research did not receive any specific funding or support from any organization. Data availability The data supporting this study are available from the corresponding authorupon reasonable request. Ethics approval and consent to participate The study protocol was approved by the Institutional Review Board of Vietnam National Children’s Hospital (IRB-VN01037/IRB0001976/FWA00028418; Approval No. 2193, September 11, 2024). The Institutional Review Board is registered with the U.S. Office for Human Research Protections (OHRP), U.S. Department of Health and Human Services. The study was conducted in accordance with the ethical standards of the Declaration of Helsinki. Consent for publication For participants aged ≥16 years, informed consent was obtained directly from the individual if they were alert and cognitively capable. For participants aged ≥16 years with impaired consciousness or cognition, as well as for all participants younger than 16 years, consent was obtained from a parent or legal guardian. Because the study population included patients with neurological impairment, consent was predominantly obtained from parents or legal guardians. Consent for publication was not applicable to this study. Conflicting Interests None References Hardy D. Autoimmune Encephalitis in Children. Pediatr Neurol . 2022;132:56-66. doi:10.1016/j.pediatrneurol.2022.05.004. Cellucci T, Van Mater H, Graus F, et al. Clinical approach to the diagnosis of autoimmune encephalitis in the pediatric patient. Neurol Neuroimmunol Neuroinflammation . 2020;7(2):e663. doi:10.1212/NXI.0000000000000663. Graus F, Titulaer MJ, Balu R, et al. A clinical approach to diagnosis of autoimmune encephalitis. Lancet Neurol . 2016;15(4):391-404. doi:10.1016/S1474-4422(15)00401-9. Lee S, Kim HD, Lee JS, Kang HC, Kim SH. Clinical Features and Treatment Outcomes of Seronegative Pediatric Autoimmune Encephalitis. J Clin Neurol . 2021;17(2):300. doi:10.3988/jcn.2021.17.2.300. Nosadini M, Thomas T, Eyre M, et al. International Consensus Recommendations for the Treatment of Pediatric NMDAR Antibody Encephalitis. Neurol - Neuroimmunol Neuroinflammation . 2021;8(5):e1052. doi:10.1212/NXI.0000000000001052. Hermetter C, Fazekas F, Hochmeister S. Systematic Review: Syndromes, Early Diagnosis, and Treatment in Autoimmune Encephalitis. Front Neurol . 2018;9:706. doi:10.3389/fneur.2018.00706. Wegener-Panzer A, Cleaveland R, Wendel EM, et al. Clinical and imaging features of children with autoimmune encephalitis and MOG antibodies. Neurol - Neuroimmunol Neuroinflammation . 2020;7(4). doi:10.1212/NXI.0000000000000731. Zeltzer L, Korner-Bitensky N, Sitcoff E, et al. Modified Rankin Scale (mRS). Stroke Engine . Evidence reviewed as of 2008 Aug 19. Gong X, Wang N, Zhu H, et al. Anti-NMDAR antibodies, the blood–brain barrier, and anti-NMDAR encephalitis. Front Neurol. 2023;14:1283511. doi:10.3389/fneur.2023.1283511. Wu CY, Wu JD, Chen CC. The Association of Ovarian Teratoma and Anti-N-Methyl-D-Aspartate Receptor Encephalitis: An Updated Integrative Review. Int J Mol Sci . 2021 Oct 9;22(20):10911. doi: 10.3390/ijms222010911. Song X, Ma J. Clinical characteristics of myelin-oligodendrocyte glycoprotein antibody-positive pediatric autoimmune encephalitis without demyelination: A case series. Front Immunol . 2022;13:1050688. doi:10.3389/fimmu.2022.105068. Jha S, Mundlamuri S’RC, Alladi S (2024). Electroencephalographic outcomes and predictors of epilepsy in autoimmune encephalitis. Seizure . 2024 Oct:121:162-171. doi: 10.1016/j.seizure.2024.08.01. Kang Q, Liao H, Yang L. Clinical Characteristics and Short-Term Prognosis of Children With Antibody-Mediated Autoimmune Encephalitis: A Single-Center Cohort Study. Front Pediatr . 2022 Jul 8;10:880693. doi: 10.3389/fped.2022.880693. Raza M, Mukhtiar K, Ibrahim S. Clinical Spectrum, Treatment and Outcome of Children with Autoimmune Encephalitis. J Coll Physicians Surg Pak . 2024;34(03):323-328. https://doi.org/10.29271/jcpsp.2024.03.323. Tables Table 1. Demographic features and history of patients with autoimmune encephalitis Features Patients AE (n = 102) NMDA (n= 60) MOG (n = 14) GABA (n = 1) Negative antibody (n = 27) Mean age at onset (years) 8.4 ± 3.9 8.8 ± 3.9 7.7 ± 4.0 13 7.6 ± 3.9 Gender (M:F) 1:1.5 1:2 1:1.3 1:0 1:0.9 Histosy (n,%) JEV 2 (2.0%) 1 (1.7%) 0 0 1 (3.7%) HSV 2 (2.0%) 2 (3.3%) 0 0 0 Cough, fever 21 (20.6%) 9 (15.0%) 3 (21.4%) 0 9 (33.3%) HFMD 1 (1.0%) 0 0 0 1 (3.7%) Data are n (%) or mean ± standard deviation values. Abbreviations: M: Male; F: Female; AE: Autoimmune encephalitis; NMDA: N-methyl-D-aspartate; MOG: Myelin oligodendrocyte glycoprotein; GABA: Gamma-aminobutyric acid; JEV: Japanese encephalitis virus; HSV: Herpes simplex virus; HFMD: Hand, foot, and mouth disease. Table 2. Paraclinical features of patients with autoimmune encephalitis Features Patients AE (n = 102) NMDA (n = 60) MOG (n = 14) GABA (n = 1) Negative antibody (n = 27) CSF (n,%) Pleocytosis (> 5/ mm 3 ) 85 (83.3%) 47 (78.3%) 13 (92.9%) 1 (100%) 24 (88.9%) Protein elevation (> 0.45g/L) 11 (10.8%) 5 (8.3%) 5 (35.7%) 0 1 (3.7%) Brain MRI (n,%) Abnormal findings 40 (39.2%) 15 (25%) 14(100%) 0 11 (40.7%) Cortical and subcortical lesions 15 (14.7%) 4 (6.7%) 7 (50%) 4 (14.8%) Basal ganglia lesions 15 (14.7%) 3 (5%) 9 (62.3%) 3 (11.1%) White matter lesions 2 (2%) 0 0 2 (7.4%) Parenchymal brain lesions 11 (10.8%) 4 (6.7%) 5 (35.7%) 2 (7.4%) Midbrain peduncle lesions 2 (2%) 0 2 (14.3%) 0 Cerebellar lesions 4 (3.9%) 0 4 (28.6%) 0 Meningeal thickening and enhancement 1 (1%) 1 (1.7%) 0 0 EEG (n,%) Abnormal findings 77 (75.5%) 45 (76.7%) 11 (78.6%) 0 20 (74.1%) Slowing of background activity 75 (73.5%) 44 (73.3%) 11 (78.6%) 0 20 (74.1%) Epileptiform discharges 12 (11.8%) 7 (11.7%) 1 (7.1%) 0 4 (14.8%) Abbreviations: AE: Autoimmune encephalitis; NMDA: N-methyl-D-aspartate; MOG: Myelin oligodendrocyte glycoprotein; GABA: Gamma-aminobutyric acid; CSF: Cerebrospinal fluid; MRI: magnetic resonance imaging; EEG: Electroencephalography. Table 3. Treatment outcomes of pediatric autoimmune encephalitis Characteristics Patients AE (n = 102) NMDA (n = 60) MOG (n = 14) GABA (n = 1) Negative antibody (n = 27) Treatment (n,%) Only Steroids 53 (52%) 28 (46.7%) 9 (64.3%) 1 (100%) 16 (59.3%) Steroids + IVIg 43 (42.2%) 28 (46.7%) 4 (28.6%) 0 11 (40.7%) Steroids + PLEX 1 (1%) 1 (1.7%) 0 0 0 Steroids + IVIg + PLEX 5 (4.9%) 4 (6.7%) 1 (7.1%) 0 0 Second-line therapy 17 (16.7%) 14 (23.3%) 2 (14.3%) 1 (100%) 0 Third-line therapy 6 (5.9%) 6 (10%) 0 0 0 Median hospital stay (days) 11 (IQR: 6-18) 11 (IQR: 6-22) 12 ± 7.1 * 5 10 (IQR: 6-17) Median mRS score at onset 2 (IQR: 1-2) 1.7 (IQR: 1-2) 1.5 (IQR: 1-3) 2 2 (IQR: 1-2) Median maximum mRS score 3.5 (IQR: 2-5) 3.5 (IQR: 2-4.8) 3.4 ± 1.4* 3 4 (IQR: 3-5) Median mRS score after 3 months 1 (IQR: 1-2) 1.7 (IQR: 0-3) 0.5 (IQR: 0-2) 2 1 (IQR: 0-1) Prognosis after 3 months (n,%) Complete recovery (mRS = 0) 34 (33.3%) 17 (28.3%) 7 (50%) 0 10 (37%) Good recovery (mRS ≤ 2) 76 (74.5%) 41 (68.3%) 11 (78.6%) 0 23 (85.2%) Partial recovery (mRS ≥ 2) 26 (25.5%) 19 (31.7%) 3 (21.4%) 1 (100%) 4 (14.8%) Data are n (%) or median (interquartile range). * mean ± standard deviation values. Abbreviations: AE: Autoimmune encephalitis; NMDA: N-methyl-D-aspartate; MOG: Myelin oligodendrocyte glycoprotein; GABA: Gamma-aminobutyric acid; IVIg: intravenous immunoglobulin; PLEX: plasma exchange; mRS: modified Rankin Scale; IQR: interquartile range. Table 4. Comparison of clinical features between the good recovery and partial recovery groups at 3 months Variables Number (n) Good recovery (%) Partial recovery (%) p-value * Female sex 61 57.9% 65.4% 0.50 NMDAR antibody positive 60 53.9% 73.1% 0.09 Seizures 59 59.2% 53.8% 0.63 Altered consciousness 40 28.9% 69.2% 0.00 Speech disorders 87 82.9% 92.9% 0.24 Behavioral abnormalities 55 47.6% 73.1% 0.02 Sleep disorders 78 73.7% 84.6% 0.26 Dyskinesia 38 27.6% 65.4% 0.001 Hypertonia 29 22.4% 46.2% 0.02 Focal neurological signs 30 30.3% 26.9% 0.75 Concomitant infection 19 11.8% 38.5% 0.003 Brain MRI abnormalities 40 39.5% 38.5% 0.69 CSF pleocytosis 85 86.8% 73.1% 0.10 Abnormal background activity on the EEG 75 68.4% 88.5% 0.046 Time from onset to peak (days) 10.1 7.1 0.29 Hospital stay (days) 11.5 36.0 0.00 Maximum mRS score 3.1 4.5 0.00 Abbreviations: CSF: Cerebrospinal fluid; MRI: magnetic resonance imaging; EEG: Electroencephalography; mRS: modified Rankin Scale. * Chi-square or Fisher’s exact test (categorical variables), t-test (continuous variables) Table 5. Multivariate logistic regression analysis Symptoms β p-value * OR 95% CI Dyskinesia 1.222 0.049 3.39 1.00 – 11.47 Maximum mRS score 0.98 0.019 2.66 1.17 – 6.00 Duration of hospitalization (days) 0.05 0.024 1.052 1.007 – 1.099 Abbreviations: OR: Odds ratio; CI: Confidence Interval * Logistic regression Additional Declarations No competing interests reported. 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1","display":"","copyAsset":false,"role":"figure","size":97546,"visible":true,"origin":"","legend":"\u003cp\u003eSee image above for figure legend.\u003c/p\u003e","description":"","filename":"Binder11.png","url":"https://assets-eu.researchsquare.com/files/rs-8062052/v1/b9bfd3e9fb13df0e0ba5f039.png"},{"id":97656667,"identity":"f40860c7-2e31-4182-bb9a-a55756710720","added_by":"auto","created_at":"2025-12-08 07:13:06","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":629855,"visible":true,"origin":"","legend":"\u003cp\u003eSee image above for figure legend.\u003c/p\u003e","description":"","filename":"Binder12.png","url":"https://assets-eu.researchsquare.com/files/rs-8062052/v1/964825e1b893896a9a5c66fb.png"},{"id":97678653,"identity":"49c236a7-e189-4e90-929a-57c79c8454e0","added_by":"auto","created_at":"2025-12-08 09:55:50","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1815564,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8062052/v1/d176da50-3421-4241-b54d-3d4bd9892926.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Clinical Characteristics and Short-Term Outcomes of Pediatric Autoimmune Encephalitis: A Single-Center Cohort Study","fulltext":[{"header":"Introduction","content":"\u003cp\u003eAutoimmune encephalitis (AE) is an immune-mediated inflammatory disorder of the brain parenchyma caused by autoantibodies targeting neuronal surface proteins, receptors, ion channels, or sometimes unidentified antigens [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Recent advances in immunological assays have led to the discovery of several specific autoantibodies, including those against myelin oligodendrocyte glycoprotein (MOG), N-methyl-D-aspartate receptor (NMDAR), leucine-rich glioma-inactivated 1 (LGI1), gamma aminobutyric acid-A (GABA), and contactin-associated protein-like 2 (CASPR2), among others [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. Among these, anti-NMDAR encephalitis is the most common subtype in children, accounting for approximately 40% of AE cases.\u003c/p\u003e\u003cp\u003eThe clinical presentation of AE is heterogeneous, typically with an acute or subacute onset of seizures, cognitive dysfunction, altered consciousness, behavioral and emotional disturbances, and sleep disorders [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. Several studies have demonstrated that distinct antibody subtypes are associated with characteristic clinical profiles, whereas a proportion of patients exhibit typical AE manifestations but remain seronegative [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. This highlights the diagnostic challenge of recognizing AE and predicting antibody subtypes in pediatric patients based solely on clinical features.\u003c/p\u003e\u003cp\u003eFirst-line immunotherapy includes high-dose corticosteroids, intravenous immunoglobulin (IVIg), or plasma exchange (PLEX). Patients who do not respond may require second-line agents such as rituximab or cyclophosphamide [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. Prognosis varies depending on the antibody subtype. Most children with anti-NMDAR encephalitis have a favorable long-term outcome, although some may experience persistent sequelae such as refractory epilepsy, memory impairment, psychiatric disorders, or even death. Patients with LGI1 antibody-associated AE typically respond rapidly to immunotherapy but may have poorer long-term outcomes than those with NMDAR antibodies. In contrast, anti-MOG AE generally shows a good response to immunotherapy and favorable recovery at discharge [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. In a study by Lee et al. (2021), 62.2% of 37 seronegative AE patients achieved good functional outcomes with modified Rankin Scale (mRS) 0\u0026ndash;1 at one-year follow-up, although the relapse rate remained high (35.1%) [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e].\u003c/p\u003e\u003cp\u003eIn Vietnam, research on autoimmune encephalitis in children remains limited, and data on the clinical characteristics, antibody profiles, and short-term outcomes are scarce. Early recognition and timely initiation of immunotherapy are crucial for improving prognosis; however, the presentation in children is often atypical, leading to diagnostic and therapeutic delays.\u003c/p\u003e\u003cp\u003eTherefore, this prospective study aimed to analyze the clinical manifestations, laboratory and neuroimaging findings, immunotherapy approaches, and short-term outcomes of children diagnosed with autoimmune encephalitis at the Vietnam National Children\u0026rsquo;s Hospital. The findings are expected to provide valuable reference data to support early diagnosis, optimize treatment strategies, and improve clinical management of autoimmune encephalitis in Vietnamese children.\u003c/p\u003e"},{"header":"Methods","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e\u003ch2\u003eStudy design\u003c/h2\u003e\u003cp\u003eThis prospective study included 102 children diagnosed with AE at the Neurology Department, Vietnam National Children\u0026rsquo;s Hospital, between August 2023 and September 2025. All patients met the diagnostic criteria for AE proposed by Cellucci et al. (2020): (1) acute or subacute onset (\u0026lt;\u0026thinsp;3 months) of neurological or psychiatric symptoms; (2) at least two signs of central nervous system dysfunction; (3) at least one paraclinical indicator of inflammation; and (4) reasonable exclusion of alternative causes [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. Patients fulfilling the diagnostic criteria for acute disseminated encephalomyelitis (ADEM) or had only the clinical criteria, without supportive paraclinical evidence of inflammation and with negative antibody findings, were excluded from the study.\u003c/p\u003e\u003c/div\u003e\n\u003ch3\u003eClinical Data Analysis\u003c/h3\u003e\n\u003cp\u003eClinical information was obtained through direct interviews with caregivers and review of medical records, including demographic characteristics, clinical manifestations, magnetic resonance imaging (MRI) findings, electroencephalography (EEG) abnormalities, cerebrospinal fluid (CSF) parameters, tumor markers, treatment modalities, and outcomes. Each patient was examined at admission and re-evaluated at 3 months post-treatment. The mRS was used to assess neurological disability, ranging from 0 (no symptoms) to 6 (death) [\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. Scores were assigned by a pediatric neurologist at disease onset, at the time of peak severity, and at 3-month follow-up. An mRS\u0026thinsp;\u0026le;\u0026thinsp;2 after 3 months was defined as a good short-term outcome, while an mRS\u0026thinsp;\u0026gt;\u0026thinsp;2 indicated partial recovery. Patients achieving an mRS of 0 were considered to have complete recovery.\u003c/p\u003e\n\u003ch3\u003eAntibody testing\u003c/h3\u003e\n\u003cp\u003eAutoantibody assays were performed on serum or cerebrospinal fluid samples, using indirect immunofluorescence assays. Tested antibodies included NMDAR, GABABR, LGI1, CASPR2, AMPA1, AMPA2, and DPPX in serum or CSF, using the autoimmune encephalitis mosaic 6 kit; while anti-MOG antibodies were analyzed in serum, using NMOSD screen 1 EUROPattern aquaporin-4 and MOG (Euroimmun). Samples were processed at the Department of Molecular Biology for Infectious Diseases, Vietnam National Children\u0026rsquo;s Hospital.\u003c/p\u003e\u003cdiv id=\"Sec6\" class=\"Section2\"\u003e\u003ch2\u003eStatistical analysis\u003c/h2\u003e\u003cp\u003eStatistical analyses were performed using SPSS software version 20.0. Normally distributed continuous variables were presented as mean\u0026thinsp;\u0026plusmn;\u0026thinsp;standard deviation and compared using the independent-samples t-test; whereas non-normally distributed variables were expressed as median and interquartile range and compared using the Mann-Whitney U test. Categorical variables were expressed as frequencies and percentages, and intergroup comparisons were made using the chi-square test or Fisher\u0026rsquo;s exact test, as appropriate. A \u003cem\u003ep\u003c/em\u003e-value\u0026thinsp;\u0026lt;\u0026thinsp;0.05 was considered statistically significant. Multivariate logistic regression was performed to identify independent predictors of poor outcome (mRS\u0026thinsp;\u0026gt;\u0026thinsp;2). Variables with p\u0026thinsp;\u0026lt;\u0026thinsp;0.1 in univariate analysis were entered into the model.\u003c/p\u003e\u003c/div\u003e"},{"header":"Results","content":"\u003cp\u003e\u003cstrong\u003eDemographic characteristics\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAmong 102 children with autoimmune encephalitis, anti-NMDAR antibodies were detected in 58.8%, anti-MOG antibodies in 13.7%, and anti-GABA antibodies in 0.9%, while 26.5% of patients were antibody-negative. Among antibody-positive patients (n = 75), anti-NMDAR AE predominated (80%), followed by anti-MOG (18.7%) and anti-GABA (1.3%). The mean age at onset of AE was 8.4 \u0026plusmn; 3.9 years, ranging from 1 to 16 years, with a male-to-female ratio of 1:1.5. The majority of patients (86.3%) were of Kinh ethnicity, with the remaining cases belonging to other ethnic groups such as Tay, Nung, Thai, Muong, and Dao. Demographic features of patients with different types of AE are summarized in Table 1.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eClinical features of pediatric autoimmune encephalitis\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAmong the 102 patients, the most common clinical manifestations were seizures, speech disorders, behavioral abnormalities, sleep disorders, and memory deficits. In the anti-NMDAR AE, the most common symptoms included speech disorders, behavioral and sleep disorders, dyskinesia, and hypertonia. Patients with anti-MOG AE more frequently presented with seizures, speech disorders, focal neurological signs, and impaired consciousness. Two patients were found to have ovarian teratomas, both of whom tested positive for anti-NMDAR antibodies. Clinical features of patients with different types of AE are summarized in Figure 1.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFigure 1.\u0026nbsp;\u003c/strong\u003eHeatmap showing the frequency of clinical manifestations in autoimmune encephalitis according to antibody subtype\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eAE: Autoimmune encephalitis; NMDA: N-methyl-D-aspartate; MOG: Myelin oligodendrocyte glycoprotein.\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eLaboratory, cerebrospinal fluid, EEG, and neuroimaging findings\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll patients in the study underwent CSF analysis, EEG, and brain MRI or computed tomography (CT) at admission. Among 102 patients, 100 patients underwent brain MRI, and 2 patients underwent CT scans. Abnormal neuroimaging findings were detected in 40 patients (39.2%). When analyzed by antibody subtype, all patients with anti-MOG AE showed abnormal brain MRI (14/14, 100%), most commonly involving the cortical, subcortical, and deep gray matter regions (Figure 2). Abnormal MRI findings were observed in 25% of patients with anti-NMDA AE and in 40.7% of antibody-negative cases, although the lesions were generally nonspecific.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFigure 2\u003c/strong\u003e.\u003cem\u003e\u0026nbsp;\u003c/em\u003eBrain MRI images on T2-FLAIR sequences of some patients with anti-MOG AE\u003c/p\u003e\n\u003cp\u003e\u003cem\u003e(A) Cortical and subcortical lesions in bilateral fronto-parietal lobes; (B) Bilateral putamen and thalamic lesions; (C) Bilateral cortical\u0026ndash;subcortical lesions; (D) Bilateral caudate nuclei, putamen, internal and external capsule lesions; (E) Cortical and thalamic lesions; (F) Bilateral putamen and thalamic lesions.\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eCSF examination was performed in all patients upon admission, revealing pleocytosis (\u0026gt; 5 cells/mm\u0026sup3;) in 83.3% and elevated protein levels (\u0026gt; 0.45 g/L) in 10.8% of cases. EEG was conducted in all patients, with abnormalities detected in 75.5%. The most common findings were diffuse or focal background slowing (72.5%), while epileptiform discharges were present in 11.8% of patients. Typical imaging and EEG findings of patients included in the study are shown in Table 2.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003e[Insert Table 2 here]\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTreatment and outcomes\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll patients in our study received first-line immunotherapy, including high-dose methylprednisolone (20 mg/kg/day for 5 days), IVIg (400 mg/kg/day for 5 days), and/or PLEX. Among them, 52% of patients were treated with methylprednisolone alone, 42.2% received a combination of methylprednisolone and IVIg, 1% were treated with IVIg and PLEX, and 4.9% received a combination of methylprednisolone, IVIg, and PLEX.\u003c/p\u003e\n\u003cp\u003eSeventeen of the 102 patients received second-line therapy with rituximab, including 14 patients with anti-NMDAR AE and 2 with anti-MOG AE. Six patients (5.9%) required third-line immunotherapy using tocilizumab or bortezomib, all of whom belonged to the anti-NMDAR AE group.\u003c/p\u003e\n\u003cp\u003eWe used the mRS to assess the clinical efficacy at disease onset, peak stage, and 3-month follow-up treatment. The mean mRS score at onset was 2 (IQR: 1-2), and the median maximum mRS score was 3.5 (IQR: 2-5). At 3 months, 74.5% of patients achieved good recovery (mRS \u0026le; 2). The proportion of good recovery was higher in patients with the anti-MOG AE (78.6%) and the antibody-negative AE (85.2%). Treatment and outcomes of patients included in the study are shown in Table 3.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003e[Insert Table 3 here]\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003e74.5% of patients achieved good recovery after 3 months (mRS \u0026le; 2). When stratified by antibody subtype, the rates of good recovery at 3 months were significantly higher in patients with anti-MOG AE and antibody-negative AE than in those with anti-NMDAR AE (78.6% and 85.2% vs. 68.3%).\u003c/p\u003e\n\u003cp\u003eAnalysis of factors associated with poor recovery showed that patients presenting with altered consciousness at admission, behavioral abnormalities, dyskinesia, hypertonia, abnormal EEG background activity, longer hospital stay, and higher mRS scores at onset and peak stage had significantly lower rates of good recovery after 3 months (\u003cem\u003ep\u003c/em\u003e \u0026lt; 0.05) (Table 4).\u003c/p\u003e\n\u003cp\u003e\u003cem\u003e[Insert Table 4 here]\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eMultivariate logistic regression analysis identified dyskinesia, higher maximum mRS score, and longer hospital stay as independent predictors of poor short-term outcome after 3 months (\u003cem\u003ep\u003c/em\u003e \u0026lt; 0.05) (Table 5).\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eOur study included 102 pediatric patients diagnosed with AE. Among antibody-positive patients (n = 75), anti-NMDAR AE predominated (80%), followed by anti-MOG (18.7%) and anti-GABA (1.3%). These findings are consistent with previous reports. In this study, the most common clinical manifestations were seizures, speech disorders, behavioral abnormalities, dyskinesia, and sleep disorders. When stratified by antibody subtype, patients with anti-NMDAR AE exhibited higher frequencies of memory deficits, behavioral abnormalities, speech disorders, dyskinesia, and hypertonia compared with other groups. In contrast, patients with anti-MOG AE typically presented with seizures, altered consciousness, and focal neurological signs, while antibody-negative AE was more often associated with seizures, speech disorders, and sleep disorders. These findings align with observations from Cellucci et al., Lee et al., and Wegener-Panzer et al [2, 4, 7].\u003c/p\u003e\n\u003cp\u003eThe clinical diversity among subtypes may be related to the specific target receptor and its functional role in neuronal signaling. The NMDAR plays a critical role in synaptic plasticity, learning, memory, and emotion regulation. Studies have shown that anti-NMDAR antibodies selectively bind to and induce internalization of surface NMDARs, leading to decreased glutamatergic synaptic transmission and resulting in neurological symptoms such as memory deficits and behavioral abnormalities [9].\u003c/p\u003e\n\u003cp\u003eThe underlying triggers of AE in children remain unclear. Several studies suggest that anti-NMDAR AE can occur following viral infections or in association with ovarian or testicular tumors. Reported viral triggers include Herpes simplex virus (HSV), Japanese encephalitis virus (JEV), and coronaviruses [1]. In our cohort, five cases developed AE following viral infections (two patients following HSV infection, two cases following JEV infection, and one case following hand-foot-and-mouth disease). In addition, 21 patients reported preceding respiratory infections within two weeks before disease onset, supporting the hypothesis that viral infections may act as potential triggers for AE.\u003c/p\u003e\n\u003cp\u003eOvarian teratoma has been recognized as an important trigger for anti-NMDAR AE, particularly in older children and young women. Previous studies reported a prevalence ranging from 1.17% to 56%, higher among adolescents and adults [10]. Therefore, screening for ovarian or testicular tumors should be considered in all pediatric patients, especially in older girls. In our study, all patients underwent abdominal ultrasound or CT, and ovarian teratomas were detected in 2% of patients, both of whom were positive for anti-NMDAR antibodies. The lower frequency in our cohort may be attributed to the younger average age (mean 8.4 ± 3.9 years) compared with other studies.\u003c/p\u003e\n\u003cp\u003eAnalysis of brain MRI findings showed abnormalities in 39.2% of patients. Abnormalities were observed in 25% of patients with anti-NMDAR AE, 100% of those with anti-MOG AE, and 40.7% of antibody-negative patients. In the anti-NMDAR group, lesions were mostly nonspecific and involved cortical or subcortical regions (6.7%), brain parenchyma (6.7%), and deep gray matter (5%). In contrast, all patients in the anti-MOG AE group demonstrated abnormal MRI findings, most commonly affecting cortical-subcortical areas (50%), deep gray matter (62.3%), brain parenchyma (35.7%), and the cerebellum (28.6%). MOG is a myelin protein located on the outer surface of the myelin sheath, distributed primarily in the white matter of the brain, spinal cord, and optic nerves. Previous studies have reported anti-MOG antibodies in acute disseminated encephalomyelitis, optic neuritis, and transverse myelitis. However, recent reports have described anti-MOG AE as an emerging clinical phenotype in children. A study from China in 2022 reported 18 pediatric patients with anti-MOG AE but without demyelinating lesions on MRI. That study noted that the most common symptoms were altered consciousness, prolonged fever, headache, seizures, and focal neurological deficits, with MRI showing T2-hyperintense lesions in the cortex, basal ganglia, thalamus, cerebellum, and brainstem [11]. Our findings are consistent with these observations, further supporting that anti-MOG AE represents a distinct clinical entity within the AE spectrum. Testing for anti-MOG antibodies should be considered in children presenting with acute neurological dysfunction and MRI abnormalities suggestive of inflammatory involvement.\u003c/p\u003e\n\u003cp\u003eAll patients underwent an EEG at admission. Abnormal EEG findings were observed in 73.5% of cases, most commonly diffuse background slowing, while epileptiform discharges were detected in 11.8%. There were no significant differences in EEG patterns among antibody subtypes. These results are consistent with those of Jha et al. (2024), who reported background slowing in approximately 82% and epileptiform activity in 25.6% of patients [12].In several cases, children presented with subtle neuropsychiatric symptoms but exhibited abnormal EEG background activity, suggesting that EEG may serve as a sensitive tool for early detection of AE in pediatric patients.\u003c/p\u003e\n\u003cp\u003eAll patients in our study received first-line immunotherapy, including steroids, IVIg, and/or PLEX. Of these, 52% were treated with steroids alone, 47.1% received combination therapy with IVIg, and 5.9% underwent PLEX. Seventeen patients (16.7%) required second-line immunotherapy with rituximab (375 mg/m² weekly for 4 weeks), while 6 patients (5.9%) required third-line therapy (2 received bortezomib and 4 received tocilizumab). Among those receiving second-line treatment, 14 (82.4%) had anti-NMDAR AE, 2 (11.8%) had anti-MOG AE, and 1 (5.9%) had anti-GABA receptor AE. All patients requiring third-line therapy were anti-NMDAR positive, indicating that this subtype tends to have more severe disease and slower recovery. In our study, one patient was diagnosed with anti-GABA AE. The patient initially presented with memory deficits and behavioral abnormalities, but was diagnosed six months after symptom onset. Despite receiving immunotherapy (steroids and rituximab), the clinical improvement was only about 50% after three months of treatment. This case highlights that delayed diagnosis and initiation of therapy may result in suboptimal recovery outcomes.\u003c/p\u003e\n\u003cp\u003eAt 3-month follow-up, the rate of good recovery (mRS ≤ 2) was lowest in the anti-NMDAR AE (68.3%), while higher recovery rates were observed in the anti-MOG AE (78.6%) and antibody-negative AE (85.2%). These findings are consistent with those reported by Lee et al. and Wegener-Panzer et al [4, 7]. Their results observed better early recovery in anti-MOG AE and antibody-negative AE, while anti-NMDAR AE often required longer recovery periods, possibly due to delayed receptor functional restoration. Several studies have shown that complete recovery from anti-NMDAR AE may take up to two years [1, 2].\u003c/p\u003e\n\u003cp\u003eSeveral clinical features, such as altered consciousness, behavioral abnormalities, and dyskinesia, were associated with a significantly higher risk of incomplete recovery compared with those without these symptoms. These findings are consistent with Kang et al. (2022), who reported that intensive care unit admission, high peak mRS scores, status epilepticus, and HSV-associated onset were predictive of poorer outcomes [13]. This suggests that severe neurological dysfunction at onset is an important indicator of poor prognosis.\u003c/p\u003e\n\u003cp\u003eBiological factors also contribute to determining outcomes. Elevated lymphocyte counts in CSF and slowing in EEG background activity indicate ongoing neuroinflammation and the degree of cortical involvement. Additionally, concurrent infections were strongly linked to unfavorable outcomes, likely by worsening the inflammatory response and extending the duration of treatment. In our cohort, longer hospital stays and higher maximum mRS scores were significantly associated with partial recovery. This suggests that the initial severity of the disease and treatment-related complications have a considerable impact on functional outcomes. On the other hand, factors such as age, sex, and MRI abnormalities showed no significant correlation in univariate analysis.\u003c/p\u003e\n\u003cp\u003eMultivariate logistic regression analysis identified dyskinesia, higher maximum mRS score, and longer hospital stay as independent predictors of poor short-term recovery. Patients with dyskinesia were approximately 3.4 times more likely to have poor recovery. Similarly, higher maximum mRS scores were strongly correlated with worse outcomes, reflecting the influence of initial disease severity on prognosis. Prolonged hospital stay also predicted unfavorable outcomes, suggesting that severe or complicated cases require longer treatment and have a lower likelihood of full recovery.\u003c/p\u003e\n\u003cp\u003ePrevious studies have shown that early initiation of therapy and the use of combination immunotherapy can lead to complete recovery without relapse [5, 6]. In our study, the rate of good recovery at 3 months was 74.3%, which is higher than the 48.2% reported by Raza M. (2024) [14]. This difference may be explained by the fact that our patients presented with milder symptoms, with a median mRS score at onset of 2 (IQR: 1 - 2) and a maximum mRS score of 3.5 (IQR: 2 - 5), whereas in Raza’s study, the median mRS score at onset was 5 (IQR: 4 - 5). However, follow-up beyond 6–12 months is necessary, as delayed neurological recovery and relapses are frequent in AE, particularly in anti-NMDAR cases. This study is limited by its single-center design, relatively short follow-up, and lack of quantitative MRI or antibody titration data, which may underestimate long-term sequelae.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003ePediatric autoimmune encephalitis in Vietnam predominantly involves anti-NMDAR antibodies and presents with diverse neurological symptoms. Most children respond well to first-line immunotherapy, yet dyskinesia, higher maximum mRS, and prolonged hospitalization predict poorer short-term recovery. Early identification and aggressive management of these risk factors may improve outcomes.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eAE \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Autoimmune encephalitis\u0026nbsp;\u003c/p\u003e\n\u003cp\u003emRS \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;modified Rankin Scale\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eMOG \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; Myelin oligodendrocyte glycoprotein\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eNMDAR \u0026nbsp; \u0026nbsp; N-methyl-D-aspartate receptor \u0026nbsp; \u0026nbsp;\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eGABA \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Gamma aminobutyric acid-A \u0026nbsp;\u003c/p\u003e\n\u003cp\u003eLGI1 \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Leucine-rich glioma-inactivated 1\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eCASPR2 \u0026nbsp; \u0026nbsp;Contactin-associated protein-like 2\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eIVIg \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Intravenous immunoglobulin\u0026nbsp;\u003c/p\u003e\n\u003cp\u003ePLEX \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; Plasma exchange\u003c/p\u003e\n\u003cp\u003eMRI \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; Magnetic resonance imaging\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eCT \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; Computed Tomography\u003c/p\u003e\n\u003cp\u003eEEG \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Electroencephalography\u003c/p\u003e\n\u003cp\u003eCSF \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Cerebrospinal fluid\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eJEV \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Japanese encephalitis virus\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eHSV \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; Herpes simplex virus\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eHFMD \u0026nbsp; \u0026nbsp; \u0026nbsp;Hand, Foot, and Mouth Disease\u003c/p\u003e\n\u003cp\u003eOR \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Odds Ratio\u003c/p\u003e\n\u003cp\u003eIQR \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Interquartile range\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eCT \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Computed Tomography\u003c/p\u003e\n\u003cp\u003eSD \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Standard Deviation\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eAcknowledgment\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors thank the clinicians and nurses at the Department of Neurology and Molecular Biology for Infectious Disease, Vietnam National Children\u0026rsquo;s Hospital, for their dedicated support in patient management and data collection.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthor Contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThi Nguyet Dao and Thanh Huong Do: Design, Writing \u0026ndash; review \u0026amp; editing, Data collection, Analysis, and Interpretation. Thi Bich Thuy Phung: Design, Methodology, Writing \u0026ndash; review \u0026amp; editing, Supervision. Thi Bich Van Nguyen, Thi Van Nguyen, and Vu Hung Cao: Data collection, Analysis.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis research did not receive any specific funding or support from any organization.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eData availability\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe data supporting this study are available from the corresponding authorupon reasonable request.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe study protocol was approved by the Institutional Review Board of Vietnam National Children\u0026rsquo;s Hospital (IRB-VN01037/IRB0001976/FWA00028418; Approval No. 2193, September 11, 2024). The Institutional Review Board is registered with the U.S. Office for Human Research Protections (OHRP), U.S. Department of Health and Human Services. The study was conducted in accordance with the ethical standards of the Declaration of Helsinki.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eFor participants aged \u0026ge;16 years, informed consent was obtained directly from the individual if they were alert and cognitively capable. For participants aged \u0026ge;16 years with impaired consciousness or cognition, as well as for all participants younger than 16 years, consent was obtained from a parent or legal guardian. Because the study population included patients with neurological impairment, consent was predominantly obtained from parents or legal guardians. Consent for publication was not applicable to this study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConflicting Interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNone\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eHardy D. Autoimmune Encephalitis in Children. \u003cem\u003ePediatr Neurol\u003c/em\u003e. 2022;132:56-66. doi:10.1016/j.pediatrneurol.2022.05.004.\u003c/li\u003e\n\u003cli\u003eCellucci T, Van Mater H, Graus F, et al. Clinical approach to the diagnosis of autoimmune encephalitis in the pediatric patient. \u003cem\u003eNeurol Neuroimmunol Neuroinflammation\u003c/em\u003e. 2020;7(2):e663. doi:10.1212/NXI.0000000000000663.\u003c/li\u003e\n\u003cli\u003eGraus F, Titulaer MJ, Balu R, et al. A clinical approach to diagnosis of autoimmune encephalitis. \u003cem\u003eLancet Neurol\u003c/em\u003e. 2016;15(4):391-404. doi:10.1016/S1474-4422(15)00401-9.\u003c/li\u003e\n\u003cli\u003eLee S, Kim HD, Lee JS, Kang HC, Kim SH. Clinical Features and Treatment Outcomes of Seronegative Pediatric Autoimmune Encephalitis. \u003cem\u003eJ Clin Neurol\u003c/em\u003e. 2021;17(2):300. doi:10.3988/jcn.2021.17.2.300.\u003c/li\u003e\n\u003cli\u003eNosadini M, Thomas T, Eyre M, et al. International Consensus Recommendations for the Treatment of Pediatric NMDAR Antibody Encephalitis. \u003cem\u003eNeurol - Neuroimmunol Neuroinflammation\u003c/em\u003e. 2021;8(5):e1052. doi:10.1212/NXI.0000000000001052.\u003c/li\u003e\n\u003cli\u003eHermetter C, Fazekas F, Hochmeister S. Systematic Review: Syndromes, Early Diagnosis, and Treatment in Autoimmune Encephalitis. \u003cem\u003eFront Neurol\u003c/em\u003e. 2018;9:706. doi:10.3389/fneur.2018.00706.\u003c/li\u003e\n\u003cli\u003eWegener-Panzer A, Cleaveland R, Wendel EM, et al. Clinical and imaging features of children with autoimmune encephalitis and MOG antibodies. \u003cem\u003eNeurol - Neuroimmunol Neuroinflammation\u003c/em\u003e. 2020;7(4). doi:10.1212/NXI.0000000000000731.\u003c/li\u003e\n\u003cli\u003eZeltzer L, Korner-Bitensky N, Sitcoff E, et al. Modified Rankin Scale (mRS). \u003cem\u003eStroke Engine\u003c/em\u003e. Evidence reviewed as of 2008 Aug 19.\u003c/li\u003e\n\u003cli\u003eGong X, Wang N, Zhu H, et al. Anti-NMDAR antibodies, the blood\u0026ndash;brain barrier, and anti-NMDAR encephalitis. Front Neurol. 2023;14:1283511. doi:10.3389/fneur.2023.1283511.\u003c/li\u003e\n\u003cli\u003eWu CY, Wu JD, Chen CC. The Association of Ovarian Teratoma and Anti-N-Methyl-D-Aspartate Receptor Encephalitis: An Updated Integrative Review. \u003cem\u003eInt J Mol Sci\u003c/em\u003e. 2021 Oct 9;22(20):10911. doi: 10.3390/ijms222010911.\u003c/li\u003e\n\u003cli\u003eSong X, Ma J. Clinical characteristics of myelin-oligodendrocyte glycoprotein antibody-positive pediatric autoimmune encephalitis without demyelination: A case series. \u003cem\u003eFront Immunol\u003c/em\u003e. 2022;13:1050688. doi:10.3389/fimmu.2022.105068.\u003c/li\u003e\n\u003cli\u003eJha S, Mundlamuri S\u0026rsquo;RC, Alladi S (2024). Electroencephalographic outcomes and predictors of epilepsy in autoimmune encephalitis. \u003cem\u003eSeizure\u003c/em\u003e. 2024 Oct:121:162-171. doi: 10.1016/j.seizure.2024.08.01.\u003c/li\u003e\n\u003cli\u003eKang Q, Liao H, Yang L. Clinical Characteristics and Short-Term Prognosis of Children With Antibody-Mediated Autoimmune Encephalitis: A Single-Center Cohort Study. \u003cem\u003eFront Pediatr\u003c/em\u003e. 2022 Jul 8;10:880693. doi: 10.3389/fped.2022.880693.\u003c/li\u003e\n\u003cli\u003eRaza M, Mukhtiar K, Ibrahim S. Clinical Spectrum, Treatment and Outcome of Children with Autoimmune Encephalitis. \u003cem\u003eJ Coll Physicians Surg Pak\u003c/em\u003e. 2024;34(03):323-328. https://doi.org/10.29271/jcpsp.2024.03.323.\u003c/li\u003e\n\u003c/ol\u003e"},{"header":"Tables","content":"\u003cp\u003e\u003cstrong\u003eTable 1.\u003c/strong\u003e Demographic features and history of patients with autoimmune encephalitis\u003c/p\u003e\n\u003ctable border=\"0\" cellspacing=\"0\" cellpadding=\"0\" width=\"666\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 172px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003cp\u003e\u003cstrong\u003eFeatures\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"5\" valign=\"top\" style=\"width: 494px;\"\u003e\n \u003cp\u003e\u003cstrong\u003ePatients\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 132px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAE\u0026nbsp;\u003cbr\u003e\u0026nbsp;(n = 102)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNMDA\u0026nbsp;\u003cbr\u003e\u0026nbsp;(n= 60)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eMOG\u003cbr\u003e\u0026nbsp; (n = 14)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 92px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eGABA\u0026nbsp;\u003cbr\u003e\u0026nbsp;(n = 1)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 87px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNegative antibody\u0026nbsp;\u003cbr\u003e\u0026nbsp;(n = 27)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 172px;\"\u003e\n \u003cp\u003eMean age at onset (years)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 132px;\"\u003e\n \u003cp\u003e8.4 \u0026plusmn; 3.9\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e8.8 \u0026plusmn; 3.9\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e7.7 \u0026plusmn; 4.0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 92px;\"\u003e\n \u003cp\u003e13\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 87px;\"\u003e\n \u003cp\u003e7.6 \u0026plusmn; 3.9\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 172px;\"\u003e\n \u003cp\u003eGender (M:F)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 132px;\"\u003e\n \u003cp\u003e1:1.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e1:2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e1:1.3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 92px;\"\u003e\n \u003cp\u003e1:0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 87px;\"\u003e\n \u003cp\u003e1:0.9\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"6\" valign=\"top\" style=\"width: 666px;\"\u003e\n \u003cp\u003eHistosy (n,%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 172px;\"\u003e\n \u003cp\u003eJEV\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 132px;\"\u003e\n \u003cp\u003e2 (2.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e1 (1.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 92px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 87px;\"\u003e\n \u003cp\u003e1 (3.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 172px;\"\u003e\n \u003cp\u003eHSV\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 132px;\"\u003e\n \u003cp\u003e2 (2.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e2 (3.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 92px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 87px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 172px;\"\u003e\n \u003cp\u003eCough, fever\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 132px;\"\u003e\n \u003cp\u003e21 (20.6%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e9 (15.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e3 (21.4%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 92px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 87px;\"\u003e\n \u003cp\u003e9 (33.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 172px;\"\u003e\n \u003cp\u003eHFMD\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 132px;\"\u003e\n \u003cp\u003e1 (1.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 92px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 87px;\"\u003e\n \u003cp\u003e1 (3.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cem\u003eData are n (%) or mean \u0026plusmn; standard deviation values.\u0026nbsp;\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eAbbreviations: M: Male; F: Female; AE: Autoimmune encephalitis; NMDA: N-methyl-D-aspartate; MOG: Myelin oligodendrocyte glycoprotein; GABA: Gamma-aminobutyric acid; JEV: Japanese encephalitis virus; HSV: Herpes simplex virus; HFMD: Hand, foot, and mouth disease.\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 2.\u0026nbsp;\u003c/strong\u003eParaclinical features of patients with autoimmune encephalitis\u003c/p\u003e\n\u003ctable border=\"0\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 165px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003cp\u003e\u003cstrong\u003eFeatures\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"5\" valign=\"top\" style=\"width: 466px;\"\u003e\n \u003cp\u003e\u003cstrong\u003ePatients\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 99px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAE\u0026nbsp;\u003cbr\u003e\u0026nbsp;(n = 102)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNMDA\u0026nbsp;\u003cbr\u003e\u0026nbsp;(n = 60)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eMOG\u0026nbsp;\u003cbr\u003e\u0026nbsp;(n = 14)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 79px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eGABA\u0026nbsp;\u003cbr\u003e\u0026nbsp;(n = 1)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNegative antibody\u003cbr\u003e\u0026nbsp;(n = 27)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"6\" valign=\"top\" style=\"width: 631px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCSF (n,%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 165px;\"\u003e\n \u003cp\u003ePleocytosis\u0026nbsp;\u003cbr\u003e(\u0026gt; 5/ mm\u003csup\u003e3\u003c/sup\u003e)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 99px;\"\u003e\n \u003cp\u003e85 (83.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e47 (78.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e13 (92.9%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 79px;\"\u003e\n \u003cp\u003e1 (100%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e24 (88.9%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 165px;\"\u003e\n \u003cp\u003eProtein elevation\u0026nbsp;\u003cbr\u003e\u0026nbsp;(\u0026gt; 0.45g/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 99px;\"\u003e\n \u003cp\u003e11 (10.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e5 (8.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e5 (35.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 79px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e1 (3.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"6\" valign=\"top\" style=\"width: 631px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eBrain MRI (n,%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 165px;\"\u003e\n \u003cp\u003eAbnormal findings\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 99px;\"\u003e\n \u003cp\u003e40 (39.2%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e15 (25%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e14(100%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 79px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e11 (40.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 165px;\"\u003e\n \u003cp\u003eCortical and subcortical lesions\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 99px;\"\u003e\n \u003cp\u003e15 (14.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e4 (6.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e7 (50%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e4 (14.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 165px;\"\u003e\n \u003cp\u003eBasal ganglia lesions\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 99px;\"\u003e\n \u003cp\u003e15 (14.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e3 (5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e9 (62.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e3 (11.1%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 165px;\"\u003e\n \u003cp\u003eWhite matter lesions\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 99px;\"\u003e\n \u003cp\u003e2 (2%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e2 (7.4%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 165px;\"\u003e\n \u003cp\u003eParenchymal brain lesions\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 99px;\"\u003e\n \u003cp\u003e11 (10.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e4 (6.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e5 (35.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e2 (7.4%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 165px;\"\u003e\n \u003cp\u003eMidbrain peduncle lesions\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 99px;\"\u003e\n \u003cp\u003e2 (2%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e2 (14.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 165px;\"\u003e\n \u003cp\u003eCerebellar lesions\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 99px;\"\u003e\n \u003cp\u003e4 (3.9%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e4 (28.6%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 165px;\"\u003e\n \u003cp\u003eMeningeal thickening and enhancement\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 99px;\"\u003e\n \u003cp\u003e1 (1%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e1 (1.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"6\" valign=\"top\" style=\"width: 631px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eEEG (n,%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 165px;\"\u003e\n \u003cp\u003eAbnormal findings\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 99px;\"\u003e\n \u003cp\u003e77 (75.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e45 (76.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e11 (78.6%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 79px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e20 (74.1%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 165px;\"\u003e\n \u003cp\u003eSlowing of background activity\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 99px;\"\u003e\n \u003cp\u003e75 (73.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e44 (73.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e11 (78.6%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 79px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e20 (74.1%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 165px;\"\u003e\n \u003cp\u003eEpileptiform discharges\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 99px;\"\u003e\n \u003cp\u003e12 (11.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e7 (11.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 93px;\"\u003e\n \u003cp\u003e1 (7.1%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 79px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e4 (14.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cem\u003eAbbreviations: AE: Autoimmune encephalitis; NMDA: N-methyl-D-aspartate; MOG: Myelin oligodendrocyte glycoprotein; GABA: Gamma-aminobutyric acid; CSF: Cerebrospinal fluid; MRI: magnetic resonance imaging; \u0026nbsp;EEG: Electroencephalography.\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 3.\u0026nbsp;\u003c/strong\u003eTreatment outcomes of pediatric autoimmune encephalitis\u003c/p\u003e\n\u003ctable border=\"0\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 141px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCharacteristics\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"5\" valign=\"top\" style=\"width: 482px;\"\u003e\n \u003cp\u003e\u003cstrong\u003ePatients\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAE\u0026nbsp;\u003cbr\u003e\u0026nbsp;(n = 102)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 95px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNMDA\u0026nbsp;\u003cbr\u003e\u0026nbsp;(n = 60)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eMOG\u0026nbsp;\u003cbr\u003e\u0026nbsp;(n = 14)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 85px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eGABA\u0026nbsp;\u003cbr\u003e\u0026nbsp;(n = 1)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 113px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNegative antibody\u003cbr\u003e\u0026nbsp;(n = 27)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"6\" valign=\"top\" style=\"width: 623px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eTreatment (n,%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 141px;\"\u003e\n \u003cp\u003eOnly Steroids\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e53 (52%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 95px;\"\u003e\n \u003cp\u003e28 (46.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e9 (64.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 85px;\"\u003e\n \u003cp\u003e1 (100%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 113px;\"\u003e\n \u003cp\u003e16 (59.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 141px;\"\u003e\n \u003cp\u003eSteroids + IVIg\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e43 (42.2%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 95px;\"\u003e\n \u003cp\u003e28 (46.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e4 (28.6%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 85px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 113px;\"\u003e\n \u003cp\u003e11 (40.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 141px;\"\u003e\n \u003cp\u003eSteroids + PLEX\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e1 (1%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 95px;\"\u003e\n \u003cp\u003e1 (1.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 85px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 113px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 141px;\"\u003e\n \u003cp\u003eSteroids + IVIg\u0026nbsp;\u003c/p\u003e\n \u003cp\u003e+ PLEX\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e5 (4.9%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 95px;\"\u003e\n \u003cp\u003e4 (6.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e1 (7.1%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 85px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 113px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 141px;\"\u003e\n \u003cp\u003eSecond-line therapy\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e17 (16.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 95px;\"\u003e\n \u003cp\u003e14 (23.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e2 (14.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 85px;\"\u003e\n \u003cp\u003e1 (100%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 113px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 141px;\"\u003e\n \u003cp\u003eThird-line therapy\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e6 (5.9%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 95px;\"\u003e\n \u003cp\u003e6 (10%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 85px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 113px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 141px;\"\u003e\n \u003cp\u003eMedian hospital stay (days)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e11\u0026nbsp;\u003cbr\u003e\u0026nbsp;(IQR: 6-18)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 95px;\"\u003e\n \u003cp\u003e11\u0026nbsp;\u003cbr\u003e\u0026nbsp;(IQR: 6-22)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e12 \u0026plusmn; 7.1\u003csup\u003e*\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 85px;\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 113px;\"\u003e\n \u003cp\u003e10\u0026nbsp;\u003cbr\u003e\u0026nbsp;(IQR: 6-17)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 141px;\"\u003e\n \u003cp\u003eMedian mRS score at onset\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e2\u0026nbsp;\u003cbr\u003e\u0026nbsp;(IQR: 1-2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 95px;\"\u003e\n \u003cp\u003e1.7\u0026nbsp;\u003cbr\u003e\u0026nbsp;(IQR: 1-2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e1.5\u0026nbsp;\u003cbr\u003e\u0026nbsp;(IQR: 1-3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 85px;\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 113px;\"\u003e\n \u003cp\u003e2\u0026nbsp;\u003cbr\u003e\u0026nbsp;(IQR: 1-2)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 141px;\"\u003e\n \u003cp\u003eMedian maximum mRS score\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e3.5\u0026nbsp;\u003cbr\u003e\u0026nbsp;(IQR: 2-5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 95px;\"\u003e\n \u003cp\u003e3.5 (IQR: 2-4.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e3.4 \u0026plusmn; 1.4*\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 85px;\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 113px;\"\u003e\n \u003cp\u003e4 (IQR: 3-5)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 141px;\"\u003e\n \u003cp\u003eMedian mRS score after 3 months\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e1\u0026nbsp;\u003cbr\u003e\u0026nbsp;(IQR: 1-2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 95px;\"\u003e\n \u003cp\u003e1.7\u0026nbsp;\u003cbr\u003e\u0026nbsp;(IQR: 0-3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e0.5\u0026nbsp;\u003cbr\u003e\u0026nbsp;(IQR: 0-2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 85px;\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 113px;\"\u003e\n \u003cp\u003e1 (IQR: 0-1)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"6\" valign=\"top\" style=\"width: 623px;\"\u003e\n \u003cp\u003e\u003cstrong\u003ePrognosis after 3 months (n,%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 141px;\"\u003e\n \u003cp\u003eComplete recovery\u0026nbsp;\u003cbr\u003e\u0026nbsp;(mRS = 0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e34 (33.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 95px;\"\u003e\n \u003cp\u003e17 (28.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e7 (50%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 85px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 113px;\"\u003e\n \u003cp\u003e10 (37%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 141px;\"\u003e\n \u003cp\u003eGood recovery\u003c/p\u003e\n \u003cp\u003e(mRS \u0026le; 2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e76 (74.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 95px;\"\u003e\n \u003cp\u003e41 (68.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e11 (78.6%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 85px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 113px;\"\u003e\n \u003cp\u003e23 (85.2%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 141px;\"\u003e\n \u003cp\u003ePartial recovery (mRS \u0026ge; 2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e26 (25.5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 95px;\"\u003e\n \u003cp\u003e19 (31.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e3 (21.4%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 85px;\"\u003e\n \u003cp\u003e1 (100%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 113px;\"\u003e\n \u003cp\u003e4 (14.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cem\u003eData are n (%) or median (interquartile range). \u003csup\u003e*\u0026nbsp;\u003c/sup\u003emean \u0026plusmn; standard deviation values.\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eAbbreviations: AE: Autoimmune encephalitis; NMDA: N-methyl-D-aspartate; MOG: Myelin oligodendrocyte glycoprotein; GABA: Gamma-aminobutyric acid; IVIg: intravenous immunoglobulin; PLEX: plasma exchange; mRS: modified Rankin Scale; IQR: interquartile range.\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 4.\u0026nbsp;\u003c/strong\u003eComparison of clinical features between the good recovery and partial recovery groups at 3 months\u003c/p\u003e\n\u003ctable border=\"0\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eVariables\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNumber (n)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eGood recovery (%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e\u003cstrong\u003ePartial recovery (%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e\u003cstrong\u003ep-value\u003csup\u003e*\u003c/sup\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eFemale sex\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e61\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e57.9%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e65.4%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.50\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eNMDAR antibody positive\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e53.9%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e73.1%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.09\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eSeizures\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e59\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e59.2%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e53.8%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.63\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eAltered consciousness\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e28.9%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e69.2%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.00\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eSpeech disorders\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e87\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e82.9%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e92.9%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.24\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eBehavioral abnormalities\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e55\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e47.6%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e73.1%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.02\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eSleep disorders\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e78\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e73.7%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e84.6%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.26\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eDyskinesia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e38\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e27.6%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e65.4%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.001\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eHypertonia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e29\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e22.4%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e46.2%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.02\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eFocal neurological signs\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e30\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e30.3%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e26.9%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.75\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eConcomitant infection\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e19\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e11.8%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e38.5%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.003\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eBrain MRI abnormalities\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e39.5%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e38.5%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.69\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eCSF pleocytosis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e85\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e86.8%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e73.1%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.10\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 198px;\"\u003e\n \u003cp\u003eAbnormal background activity on the EEG\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 104px;\"\u003e\n \u003cp\u003e75\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e68.4%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e88.5%\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.046\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"2\" valign=\"top\" style=\"width: 302px;\"\u003e\n \u003cp\u003eTime from onset to peak (days)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e10.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e7.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.29\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"2\" valign=\"top\" style=\"width: 302px;\"\u003e\n \u003cp\u003eHospital stay (days)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e11.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e36.0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.00\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"2\" valign=\"top\" style=\"width: 302px;\"\u003e\n \u003cp\u003eMaximum mRS score\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e3.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 123px;\"\u003e\n \u003cp\u003e4.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 76px;\"\u003e\n \u003cp\u003e0.00\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cem\u003eAbbreviations: CSF: Cerebrospinal fluid; MRI: magnetic resonance imaging; \u0026nbsp;EEG: Electroencephalography; mRS: modified Rankin Scale.\u003cbr\u003e \u003csup\u003e*\u003c/sup\u003eChi-square or Fisher\u0026rsquo;s exact test (categorical variables), t-test (continuous variables)\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 5.\u0026nbsp;\u003c/strong\u003eMultivariate logistic regression analysis\u003c/p\u003e\n\u003ctable border=\"0\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 129px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eSymptoms\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u0026beta;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e\u003cstrong\u003ep-value\u003csup\u003e*\u003c/sup\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eOR\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 115px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e95% CI\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 129px;\"\u003e\n \u003cp\u003eDyskinesia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e1.222\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e0.049\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e3.39\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 115px;\"\u003e\n \u003cp\u003e1.00 \u0026ndash; 11.47\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 129px;\"\u003e\n \u003cp\u003eMaximum mRS score\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e0.98\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e0.019\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e2.66\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 115px;\"\u003e\n \u003cp\u003e1.17 \u0026ndash; 6.00\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 129px;\"\u003e\n \u003cp\u003eDuration of hospitalization (days)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e0.05\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e0.024\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 126px;\"\u003e\n \u003cp\u003e1.052\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 115px;\"\u003e\n \u003cp\u003e1.007 \u0026ndash; 1.099\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cem\u003eAbbreviations: OR: Odds ratio; CI: Confidence Interval\u003cbr\u003e \u003csup\u003e*\u003c/sup\u003eLogistic regression\u003c/em\u003e\u003c/p\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":"autoimmune encephalitis, clinical features, short-term outcomes, pediatric","lastPublishedDoi":"10.21203/rs.3.rs-8062052/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8062052/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eObjective\u003c/h2\u003e\u003cp\u003eThe study aimed to investigate the clinical characteristics and short-term outcomes of children with autoimmune encephalitis (AE) in North Vietnam.\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e\u003cp\u003eWe conducted a prospective cohort study of 102 children diagnosed with AE at the Vietnam National Children\u0026rsquo;s Hospital between August 2023 and September 2025 based on Cellucci et al. criteria 2020. Demographic, clinical, laboratory, neuroimaging, and antibody data were collected. Short-term (3-month) outcomes were assessed using the modified Rankin Scale (mRS) by the pediatric neurologist. The children were divided into good (scores\u0026thinsp;\u0026le;\u0026thinsp;2) and poor (scores\u0026thinsp;\u0026gt;\u0026thinsp;2).\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e\u003cp\u003eThe mean age was 8.4\u0026thinsp;\u0026plusmn;\u0026thinsp;3.9 years, with a male-to-female ratio of 1:1.5. Anti-NMDAR AE accounted for 80% of antibody-positive cases, followed by anti-MOG (18.7%) and anti-GABA (1.3%). The most common symptoms were speech disorders (85.3%), sleep disorders (76.5%), seizures (57.8%), and behavioral abnormalities (53.9%). At 3 months, 74.5% achieved good recovery (mRS\u0026thinsp;\u0026le;\u0026thinsp;2), with higher rates in anti-MOG (78.6%) and antibody-negative (85.2%) groups, and the lowest in anti-NMDAR AE (68.3%). Independent predictors of poor outcome included dyskinesia (OR 3.39, p\u0026thinsp;=\u0026thinsp;0.049), higher maximum mRS (OR 2.66, p\u0026thinsp;=\u0026thinsp;0.019), and longer hospitalization (OR 1.05 per day, p\u0026thinsp;=\u0026thinsp;0.024).\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e\u003cp\u003ePediatric AE shows heterogeneous presentations, predominantly anti-NMDAR AE, which tends to be more severe. Early recognition of prognostic indicators may improve treatment strategies.\u003c/p\u003e","manuscriptTitle":"Clinical Characteristics and Short-Term Outcomes of Pediatric Autoimmune Encephalitis: A Single-Center Cohort Study","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-12-08 07:13:01","doi":"10.21203/rs.3.rs-8062052/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"editorInvitedReview","content":"","date":"2025-12-14T19:00:01+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-12-14T08:54:04+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-12-11T12:19:48+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-12-08T14:36:25+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"116679037171108347407187876186879675673","date":"2025-12-05T06:02:07+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"63476757870801296893596265021370796227","date":"2025-12-04T09:30:02+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"50661639364742611276269213458635458061","date":"2025-12-04T01:17:08+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"334584179602650654904179206991861438790","date":"2025-12-03T23:21:22+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-12-03T04:42:26+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-12-03T04:34:08+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2025-12-01T23:41:49+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-12-01T13:52:09+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Neurology","date":"2025-12-01T13:18:11+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":"beda1efe-76d9-45a3-9fc4-01db032b742e","owner":[],"postedDate":"December 8th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2025-12-08T07:13:01+00:00","versionOfRecord":[],"versionCreatedAt":"2025-12-08 07:13:01","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8062052","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8062052","identity":"rs-8062052","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}