To summarize the clinical features and management of severe sinoatrial node dysfunction in anti-N-methyl-D-aspartate (NMDA) receptor encephalitis, and to raise awareness of this rare but life-threatening complication. We retrospectively analyzed three patients with anti-NMDA receptor encephalitis who developed sinus arrest and reviewed similar published cases. PubMed, Web of Science Core Collection, and Google Scholar were searched for reports published between January 2005 and January 2025 using the terms “anti-N-methyl-D-aspartate receptor encephalitis,” “anti-NMDAR encephalitis,” “cardiac arrest,” “sinus node dysfunction,” “sinus arrest,” “sinus pause,” and “asystole.” Only cases with confirmed anti-NMDAR encephalitis, documented cardiac rhythm abnormalities, and sufficient clinical data were included. In our three patients, sinus arrest lasted 5.71, 9.23, and 6.20 s, occurring on hospital days 17, 6, and 15, respectively. One patient underwent teratoma resection and received a temporary pacemaker. All three patients regained normal sinus rhythm after immunotherapy and achieved favorable clinical outcomes. The literature review identified 25 additional cases. In a pooled cohort of 28 patients, most were young women; sinus arrest often coincided with seizures and generally manifested during the acute phase. Overall, 76.92

BACKGROUND:Temporal lobe epilepsy (TLE) is characterized by synaptic dysfunction for which targeted therapies are lacking. Hydroxysteroid dehydrogenase-like 2 (HSDL2) was previously identified as a potential regulator in TLE, but its precise functional and mechanistic role remained unexplored. METHODS:We compared HSDL2 protein expression in cortical tissues from patients with drug-resistant TLE and a kainic acid (KA)-induced mouse model via western blotting. Cellular localization was determined by immunofluorescence co-staining with neuronal (NeuN and PSD95), astrocytic (GFAP), and microglial (IBA1) markers. Adeno-associated virus (AAV) vectors were used to overexpress or knock down HSDL2 in the mouse hippocampus, followed by behavioral seizure assessments using pentylenetetrazol (PTZ) and chronic monitoring of spontaneous recurrent seizures (SRS). Underlying mechanisms were investigated through protein-protein interaction, patch-clamp electrophysiology, and quantitative co-immunoprecipitation. RESULTS:HSDL2 was significantly upregulated in both human TLE foci and the KA-induced epileptic mouse brain. It was localized to both neurons and astrocytes. In vivo, HSDL2 overexpression prolonged the latency to PTZ-induced seizures and reduced SRS frequency, whereas its knockdown exacerbated seizure severity and duration. Mechanistically, HSDL2 enhanced the membrane localization of postsynaptic density protein 95 (PSD95) and promoted its phosphorylation. This modification disrupted the physical interaction between PSD95 and the N-methyl-D-aspartate receptor (NMDAR) NR2B and NR2A subunits, leading to a reduction in NMDAR-mediated synaptic currents and neuronal hyperexcitability. CONCLUSIONS:Our findings identify HSDL2 as a novel endogenous antiseizure protein that confers protection in epilepsy by modulating synaptic excitability. Specifically, HSDL2 regulates the PSD95-NMDAR complex through post-translational modification of PSD95, thereby inhibiting excessive NMDAR activity. Its therapeutic modulation may offer a strategy for drug development in TLE.

Abstract Background Stroke, a leading cause of morbidity and mortality worldwide, is a cerebrovascular disorder characterized by acute brain injury due to cerebral blood vessel occlusion or rupture. Post-stroke cerebral edema significantly contributes to poor prognosis, yet effective preventive therapies remain limited. Recent studies suggest that glibenclamide exhibits anti-edema and neuroprotective properties in central nervous system (CNS) injuries, showing promise in experimental stroke models. Methods A systematic search of PubMed, Web of Science, Embase, and Scopus was conducted from their inception to April 5, 2025. Search terms included “glibenclamide” combined with “stroke”, “cerebral infarction”, “cerebral hemorrhage”, or “subarachnoid hemorrhage”. A favorable outcome was defined as the modified Rankin Scale (mRS) scores 0–2 at 90 days, which served as the primary outcome. Secondary outcomes included the incidence of hypoglycemia, pneumonia, decompressive craniectomy, cardiac events, mortality, and serious adverse events. Results Seven studies involving a total of 1,225 participants were included. Regarding the primary outcome, no statistically significant difference was observed (odds ratio [OR] = 1.25, 95% confidence interval [CI] 0.92 to 1.70; P = 0.15). For secondary outcomes, glibenclamide treatment was associated with a significantly increased risk of hypoglycemic events (OR = 3.83, 95% CI 1.12 to 13.14; P = 0.03). However, there were no statistically significant differences in the incidence of pneumonia, decompressive craniectomy, cardiac events, mortality, or serious adverse events. Conclusion Current evidence does not support the efficacy of glibenclamide in improving post-stroke neurological function. Furthermore, its administration is associated with an elevated risk of hypoglycemia. Therefore, glibenclamide is not recommended for routine clinical use in this population. Registration number CRD420251024136.

Abstract Temporal lobe epilepsy (TLE) is a complex neurological disorder characterized by spontaneous recurrent seizures and its underlying mechanism remains elusive. This study aimed to investigate the role of cystine-knot AMPAR modulating protein 44 (CKAMP44) in the pathological process of TLE and its potential as a therapeutic target using kainic acid (KA)-induced epilepsy mouse model of TLE. Our results showed that CKAMP44 protein and mRNA expression was significantly increased and primarily localized to neurons during the chronic phase of TLE. Nkx2-1 regulated the transcription of CKAMP44 in the hippocampus brain tissues of KA-induced TLE mice. Inhibition of CKAMP44 suppressed seizure susceptibility and severity in the KA-induced epilepsy mice via behavioral and local field potential monitoring. Furthermore, inhibition of CKAMP44 decreased frequency and amplitudes of spontaneous excitatory postsynaptic currents indicating that the excitatory synaptic transmission was reduced in an in vitro epilepsy model. Mechanistically, inhibition of CKAMP44 specifically upregulated the membrane surface expression of GluA1 and the phosphorylation level of GluA1-ser831 by downregulating protein phosphatase 3 regulatory subunit B(PPP3r2) expression. Overexpression of PPP3r2 downregulated the phosphorylation level and surface expression of GluA1, which ultimately exacerbated the seizure activity suppressed by CKAMP44 knockdown. Collectively, our results indicate that CKAMP44 may be a potential therapeutic target for the treatment of TLE.

OBJECTIVE:This study aimed to develop and validate machine learning (ML) models for predicting the prognosis of status epilepticus (SE) patients with multisystem complications. METHODS:We developed predictive models using six ML algorithms: least absolute shrinkage and selection operator (LASSO) logistic regression, k-nearest neighbors (KNN), support vector machine (SVM), decision tree (DT), random forest (RF), and extreme gradient boosting (XGBoost). We systematically evaluated the prognostic performance of these models against established clinical scores. Specifically, we compared them with the Status Epilepticus Severity Score (STESS), the Encephalitis-Nonconvulsive Status Epilepticus-Diazepam Resistance-Imaging Abnormalities-Tracheal Intubation (ENDIT) score, and the Epidemiology-based Mortality Score in Status Epilepticus (EMSE). RESULTS:A total of 169 patients with SE were included in this study. In the test dataset, the areas under the curve (AUC) of the models were 0.660 for DT, 0.644 for RF, 0.663 for SVM, 0.689 for KNN, 0.825 for XGBoost, and 0.610 for LASSO logistic regression.The SHAP analysis revealed the top ten predictors contributing to the XGBoost model: hypoalbuminemia, nutritional risk score, age, ventilation duration, NCSE, GCS score, duration of impaired consciousness, creatinine level, APACHE II score, and CCI. CONCLUSION:Compared with the other models and scoring systems, XGBoost demonstrated superior predictive performance, suggesting its potential utility for the early identification of high-risk patients and timely clinical intervention. Hypoalbuminemia was identified as the most important prognostic factor, highlighting the critical role of systemic injury in determining adverse outcomes in SE patients treated within the neurocritical care setting.

BACKGROUND:Patients with epilepsy frequently experience comorbid anxiety and depressive symptoms. While polytherapy is known to increase depressive risk in epilepsy, it remains unclear whether social environments modify this association. OBJECTIVE:To examine the association between antiseizure medication burden and emotional states (anxiety and depression), and to evaluate whether urban-rural residence moderates this relationship. METHODS:A total of 406 patients with epilepsy were included. Anxiety and depression were assessed using the GAD-7 and C-NDDI-E. Three multiple linear regression models were constructed: Model 1 (ASM count only), Model 2 (adjusted for variables with p < 0.10 in univariate analyses), and Model 3 (fully adjusted). The interaction between residence and the number of ASMs was tested, and simple effects were examined using estimated marginal means. Sensitivity analyses were performed to assess robustness. RESULTS:The number of ASMs was positively associated with both anxiety and depression scores (both p < 0.001). In the fully adjusted model, a significant interaction was observed between residential setting and the number of ASMs for depression (β = 2.379, p < 0.01), whereas no such interaction was found for anxiety Sensitivity analyses yielded consistent results, with the interaction effect remaining stable across models. CONCLUSION:The number of ASMs is significantly associated with emotional states in patients with epilepsy, and its impact on depression is moderated by residential setting. Polytherapy confers a more pronounced detrimental effect on depressive symptoms among rural patients.

Ubiquilin 4 (UBQLN4) is an important molecule that regulates protein degradation through the ubiquitin-proteasome pathway. This study found that UBQLN4 expression is significantly reduced in a chronic epilepsy mouse model induced by kainic acid, primarily localized in neurons and widely distributed at excitatory post-synapses. Experiments involving adeno-associated virus-mediated overexpression or knockdown of UBQLN4 indicate that a reduction in UBQLN4 increases susceptibility to and severity of epilepsy, while its overexpression has a protective effect. Mechanistic studies show that UBQLN4 regulates the degradation of the N-Methyl d-Aspartate 2B Subunit (GluN2B) via the proteasome pathway, thereby affecting synaptic function. This research reveals the critical role of UBQLN4 in epilepsy and provides a potential new target for the treatment of epilepsy.

Epilepsy is a common chronic neurological condition, and temporal lobe epilepsy (TLE) is the most common form of refractory epilepsy. However, the underlying causes of TLE remain unclear. Our initial findings revealed that the expression of sorting nexin 14 (SNX14), which is a member of the sorting nexin protein family, was significantly upregulated in brain tissues from both patients with TLE and mouse models of TLE. Moreover, modulation of SNX14 expression in the hippocampus of mice demonstrated that SNX14 downregulation significantly decreased the susceptibility to and severity of seizures, whereas SNX14 overexpression exerted the opposite effects. Mechanistically, we revealed that GluA2, which is a subunit of the α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptor, was a downstream target of SNX14. Further studies indicated that SNX14 modulated GluA2 protein levels by regulating GluA2 degradation via the lysosomal pathway, which in turn influenced glutamatergic synaptic transmission. In conclusion, our findings suggest that the SNX14-GluA2 pathway could be a promising target for the development of novel treatments for epilepsy.

Background and Objectives:This study aimed to investigate the association between hydration status and 90-day functional outcomes in patients with spontaneous intracerebral hemorrhage (SICH). Methods:We conducted a retrospective analysis of 215 SICH patients admitted to the Neurology Department of the First Affiliated Hospital of Chongqing Medical University between January 2021 and September 2023. Demographic characteristics, imaging findings, and laboratory parameters were collected. Patients were stratified into good (modified Rankin Scale [mRS] ≤ 2) and poor (mRS > 2) prognosis groups based on 90-day outcomes. Results:Univariate analysis revealed that poor prognosis was associated with advanced age, prolonged hospitalization, and elevated urea nitrogen/creatinine ratio (UCR) on day 7 (p < 0.05). Multivariate logistic regression identified three independent predictors of poor outcome: age (OR = 1.059, 95% CI [1.025-1.094], p < 0.01), Glasgow Coma Scale score (OR = 0.420, 95% CI [0.308-0.571], p < 0.01), and day-7 UCR (OR = 1.095, 95% CI [1.045-1.148], p < 0.01). Receiver operating characteristic (ROC) analysis demonstrated that day-7 UCR predicted poor outcomes with an area under the curve (AUC) of 0.72 (95% CI [0.643-0.789]), with an optimal cutoff value of 30.68. Patients with UCR ≤ 30.68 had significantly higher rates of favorable outcomes (75.2%) compared to those with UCR > 30.68 (37.9%). Conclusion:Elevated blood UCR (>30.68) on day 7 post-SICH is an independent predictor of unfavorable short-term prognosis.

OBJECTIVE:Memory impairment, particularly subjective memory complaints, is common among patients with epilepsy and significantly affects their quality of life and treatment adherence. This study aimed to investigate the factors influencing subjective memory in epilepsy, with a specific focus on the roles of psychological resilience and perceived stress, and to examine whether perceived stress mediates the relationship between psychological resilience and subjective memory. METHODS:A total of 145 patients with epilepsy were prospectively enrolled at the Epilepsy Center of a tertiary teaching hospital. Comprehensive assessments were conducted to evaluate psychological resilience, perceived stress, subjective and objective memory performance, and demographic and clinical characteristics. Statistical analyses included Pearson or Spearman correlation, group comparisons, and multiple regression analyses to identify the influencing factors. The mediation effects were tested using the bootstrap method with 5000 resamples. RESULTS:Subjective memory was positively correlated with psychological resilience (r = .441, p < .001) and negatively correlated with perceived stress (r = -.574, p < .001). Regression analysis indicated that psychological factors remained significant predictors after controlling for the relevant covariates. Mediation analysis demonstrated that perceived stress exerted a significant indirect effect on the association between psychological resilience and subjective memory (ACME = .1554, 95% CI [.03, .31], p = .015), which accounted for 32.96% of the total effect. SIGNIFICANCE:Psychological resilience and perceived stress are significant contributors to subjective memory in epilepsy. The mediating role of perceived stress suggests its potential as a target for psychological intervention.

Anti-GABAB receptor encephalitis coexistence with autoimmune polyendocrine syndrome (APS) has not been reported. We present the first case of anti-GABAB receptor encephalitis coexisting with APS type III. A 64-year-old male presented with recurrent convulsions with loss of consciousness. Diagnostic evaluation revealed positive anti-GABAB receptor antibodies, elevated HbA1cand fasting blood glucose, and glutamic aciddecarboxylase antibodies (GAD-Ab), hypothyroidism with positive thyroglobulin and peroxidase antibody. The patient demonstrated complete diagnostic criteria for both anti-GABAB receptor encephalitis and APS type III. A Combination therapy with pulse corticosteroids, intravenous immunoglobulin, levothyroxine, and insulin achieved significant clinical improvement. The findings expand the spectrum of autoimmune overlap syndromes and highlight diagnostic challenges in patients presenting with concurrent neurological and endocrine dysfunction.

OBJECTIVE:We aimed to establish a quantitative electroencephalography-based prognostic prediction model specifically tailored for nontraumatic coma patients to guide clinical work. METHODS:This retrospective study included 126 patients with nontraumatic coma admitted to the First Affiliated Hospital of Chongqing Medical University from December 2020 to December 2022. Six in-hospital deaths were excluded. The Glasgow Outcome Scale assessed the prognosis at 3 months after discharge. The least absolute shrinkage and selection operator regression analysis and stepwise regression method were applied to select the most relevant predictors. We developed a predictive model using binary logistic regression and then presented it as a nomogram. We assessed the predictive effectiveness and clinical utility of the model. RESULTS:After excluding six deaths that occurred within the hospital, a total of 120 patients were included in this study. Three predictor variables were identified, including APACHE II score [39.129 (1.4244-1074.9000)], sleep cycle [OR: 0.006 (0.0002-0.1808)], and RAV [0.068 (0.0049-0.9500)]. The prognostic prediction model showed exceptional discriminative ability, with an AUC of 0.939 (95 % CI: 0.899-0.979). CONCLUSION:A lack of sleep cycles, smaller relative alpha variants, and higher APACHE II scores were associated with a poor prognosis of nontraumatic coma patients in the neurointensive care unit at 3 months after discharge. CLINICAL IMPLICATION:This study presents a novel methodology for the prognostic assessment of nontraumatic coma patients and is anticipated to play a significant role in clinical practice.

Background Malaria is an infectious malady caused by Plasmodium parasites, cerebral malaria standing out as one of its most severe complications. Clinical manifestation include elevated body temperature, loss of consciousness, and seizures. However, reports of cerebral malaria presenting as nonconvulsive status epilepticus are extremely rare. The case presented involves psychiatric symptoms, with the electroencephalogram indicated nonconvulsive status epilepticus associated with cerebral malaria. Case presentation A 53-year-old male, was urgently admitted, due to confusion and abnormal behaviour for 10 h. The patient returned to China after developing a fever while working in Tanzania two months ago. The blood smear revealed Plasmodium vivax and Plasmodium falciparum , and he was diagnosed with malaria. He recovered following anti-malarial treatment. After admission, the patient was confused, unable to communicate normally, and unwilling to cooperate with the physical examination. Plasmodium was not found in the blood smear, but the DNA sequence of P. falciparum was discovered using metagenomic next-generation sequencing of cerebrospinal fluid. Brain MRI revealed no significant abnormalities. Continuous electroencephalogram monitoring revealed that the patient had non-convulsive status epilepticus, which was treated with diazepam and levetiracetam. The patient had normal consciousness and behaviour. He received anti-malarial treatment for two weeks and fully recovered. Conclusions This case demonstrates that nonconvulsive status epilepticus can be a manifestation of cerebral malaria. It is imperative for attending physicians to heighten vigilance when encountering patients with a history of travel to malaria-endemic regions or a prior malaria infection, especially in the presence of unusual clinical presentations.

Background: BTK inhibitors (BTKis) have become the standard-of-care therapies for both frontline and relapsed/refractory Chronic Lymphocytic Leukemia /Small Lymphocytic Lymphoma (CLL/SLL). As a second-generation BTKi, zanubrutinib has demonstrated superior efficacy and a favorable safety profile in head-to-head clinical trials compared to the first-generation BTKi, ibrutinib. The objective of this study was to assess the real-world efficacy of single-agent zanubrutinib in patients with CLL/SLL. This study presents the largest multicenter, real-world data on zanubrutinib monotherapy in Chinese CLL/SLL patients (NCT06489184). Methods: This was a retrospective observational study of adult patients with CLL/SLL who initiated single-agent zanubrutinib treatment between June 2014 and March 2024 at fourteen sites across China, followed up through April 1, 2024. All patients had at least one month of follow-up. Duration of treatment (DOT), reasons for discontinuation, real-world progression-free survival (rwPFS), overall survival (OS), and dose reduction were reported. Results: A total of 322 patients received zanubrutinib monotherapy in the first line (1L, n = 180), second line (2L, n = 105), and third line or greater (≥3L, n = 36), and included one patient for whom the treatment line was unknown. The median (range) age of patients was 64.7 (34-92) years, and most patients were male (63%). Moreover, del(17p) or TP53 mutation was found in 62/266 (23.3%) tested patients. Unmutated IGHV was reported in 116/222 (52%). After a median (range) follow-up of 25.0 (1.0-119.3) months, 20.3% of patients discontinued zanubrutinib, mostly due to progressive disease (31 patients, 9.6%). Seventeen patients (5.3%) discontinued treatment due to patient preference, and 14 patients (4.3%) discontinued treatment due to adverse events (AEs). The most common AEs leading to discontinuation were infections (including COVID-19) (1.6%) and bleeding (1.3%). No cardiac AEs led to discontinuation; only one patient discontinued treatment due to blood pressure elevated. A total of 255 patients were still on zanubrutinib treatment. The 24-month duration of treatment rate was 84.4% in all patients (1L: 88.4%, 2L: 87.4%, ≥3L: 64.3%). The 24-month rwPFS rates were 95.9% for 1L, 90.8% for 2L, and 78.9% for ≥3L, while the OS rates were 97.4%, 96.3%, and 89.1%, respectively. Fifty-seven patients initiated zanubrutinib before June 2020 (when zanubrutinib was approved in China for CLL/SLL therapy on June 3, 2020), 12 patients in 1L, 30 patients in 2L, 15 patients in 3L, being patients from clinical trials. The median DOT of these patients was 71.6 months, and their median rwPFS were 109.6 months, 72-month rwPFS rate was 60.4%, the median OS has not been reached, and the 72-month OS rate were 86.3% . Dose reduction due to AEs occurred in 12 patients; among them, 4 patients experienced platelet count decreased, 3 patients experienced bleeding, and 2 patients experienced cardiac AEs (one with palpitations and atrioventricular block first degree, and one with paroxysmal atrial tachycardia and atrial fibrillation). Conclusion: The real-world efficacy of zanubrutinib monotherapy for CLL/SLL is consistent with clinical trials. These results strongly support zanubrutinib as a valuable treatment option for CLL/SLL patients, especially in those receiving first-line therapy, and discontinuation and dose reduction due to cardiac AEs are less common. Further investigation is warranted to fully elucidate the long-term benefits of zanubrutinib in the management of CLL/SLL.

INTRODUCTION:Whether in neurology or dentistry, odontogenic brain abscess stands as an ailment demanding undivided attention. The onset of this disease is insidious, with a relatively low incidence rate but a markedly high fatality rate. Moreover, its symptoms lack specificity, easily leading to misdiagnosis, oversight, and treatment delays. Hence, clinicians should maintain heightened vigilance when faced with pathogenic bacteria of dental origin in patients. AREAS COVERED:This paper encapsulates the latest research findings on the clinical manifestations and essential treatment points of odontogenic brain abscess. It may offer a crucial reference for prompt diagnosis and improved therapeutic approaches. EXPERT OPINIONS:Odontogenic brain abscess, an infection of the cerebral parenchyma, usually appears in immunocompromised patients with dental ailments or postdental surgeries. The main pathogenic microorganisms include Streptococcus intermedius, Fusobacterium nucleatum, Streptococcus anginosus, and Millerella. Given the undetectable and nonspecific symptoms in patients, the diagnostic process relies on microbiological methods. Therefore, clinicians should actively investigate and identify the pathogenic microorganisms of odontogenic brain abscess for early detection and selection of appropriate treatment regimens to avoid disease management delays.

Long-term biopotential monitoring requires high-performance biocompatible wearable dry electrodes. But currently, it is challenging to establish a form-preserving fit with the skin, resulting in high interface impedance and motion artifacts. This research aims to present an innovative solution using an all-green organic dry electrode that eliminates the aforementioned challenges. The dry electrode is prepared by introducing biocompatible maltitol into the chosen conductive polymer, poly(3,4-ethylenedioxythiophene):poly(styrenesulfonate). Thanks to the secondary doping and plasticizer effect of maltitol, the dry electrode exhibits good stretchability (62%), strong self-adhesion (0.46 N/cm), high conductivity (102 S/cm), and low Young's modulus (7 MPa). It can always form a conformal contact with the skin even during body movements. Together with good electrical properties, the electrode enables a lower skin contact impedance compared to the current standard Ag/AgCl gel electrode. Consequently, the application of this dry electrode in bioelectrical signal measurement (electromyography, electrocardiography, electroencephalography) and long-term biopotential monitoring was successfully demonstrated.

BackgroundHuman herpesvirus (HHV)-6 encephalitis secondary to chimeric antigen receptor (CAR)-T cell therapyis relatively rare in clinical practice and needs to be differentiated from immune effector cell-associatedneurotoxicity syndrome (ICANS).MethodsWe retrospectively reported a case of HHV-6 encephalitis secondary to CAR-T cell therapy.ResultsA male patient from China with diffuse large B-cell lymphoma underwent chimeric CAR-T cell therapy anddeveloped a generalized rash on the 8th day, followed by cognitive changes, memory loss, and disorientation onthe 14th day after CAR-T cell therapy. Initially, ICANS was suspected. A lumbar puncture was performed on the 18th day. The cerebrospinal fluid (CSF) analysis revealed slightly elevated protein levels and a high presence of HHV-6B sequences by mNGS. Brain MRI showed bilateral hippocampal abnormalities. The patient was ultimatelydiagnosed with HHV-6 encephalitis and treated with ganciclovir and dexamethasone. After one week of treatment,follow-up CSF analysis showed a reduction in HHV-6B sequences. The patient was discharged with improvedmemory and orientation.ConclusionHHV-6 encephalitis secondary to CAR-T cell therapy may be easily confused with ICANS. Timely andaggressive diagnostic procedures, such as mNGS of CSF and cranial imaging, along with prompt antiviral therapy,are crucial for improving patient outcomes.

OBJECTIVE:Patients diagnosed with autoimmune encephalitis (AE) require admission to the neurological intensive care unit (ICU) when they exhibit clinical manifestations such as status epilepticus, central hypoventilation, and severe involuntary movements. In order to determine the predictors of ICU admission and prognosis for patients with AE admitted to the neurological ICU, we analyzed the clinical characteristics of this patient population.METHODS:This retrospective study analyzed 123 patients admitted to the First Affiliated Hospital of Chongqing Medical University between 2012 and 2021 who were diagnosed with AE based on serum and/or cerebrospinal fluid (CSF) AE-related antibody positivity. We divided these patients into two groups: those who received ICU treatment and those who did not. We evaluated patient's prognosis using the modified Rankin scales (mRS).RESULTS:Univariate analysis revealed that epileptic seizures, involuntary movements, central hypoventilation, symptoms of vegetative neurological disorders, increased neutrophil-to-lymphocyte ratio (NLR), abnormal electroencephalogram (EEG) findings, and different treatments were associated with ICU admission for patients with AE. Multivariate logistic regression analysis showed that hypoventilation and NLR were independent risk factors for ICU admission in AE patients. Univariate analysis showed that age and sex were related to prognosis in ICU-treated AE patients, and logistic regression analysis indicated that age was the only independent risk factor for prognosis in ICU-treated AE patients.CONCLUSION:Increased NLR, except for hypoventilation, is an indicator of ICU admission in AE patients. Although a large number of patients with AE require ICU admission, the overall prognosis is good, particularly in younger patients.