Stroke remains a major global public health challenge, with persistent disparities in its burden across countries, and an increasing burden among young adults aged 15-49 has emerged as a growing concern. However, comprehensive evaluations of stroke and its subtypes among young adults in Asia remain limited. This study utilizes data from the 2021 Global Burden of Diseases, Injuries, and Risk Factors Study (GBD), covering the period from 1990 to 2021, to assess the burden of stroke in Asia and provide evidence-based policy and resource allocation. In this study, we extracted GBD 2021 data to estimate the absolute numbers and rates of prevalence, incidence, mortality, disability-adjusted life years (DALYs), years of life lost (YLLs), and years lived with disability (YLDs) due to stroke and its subtypes among young adults (15-49 years) in Asia from 1990 to 2021, with data stratified by year, age group, and sex. In addition, we analyzed major risk factors and projected future trends through 2050. Our analysis showed that in 2021, stroke accounted for 14.70 million (95% UI 13.39–16.01 million) DALYs and 1.14 million (95% UI 0.99–1.32 million) new cases in Asia, with a DALY rate of 620.24 (95% UI 564.66–675.12) per 100,000 and an incidence rate of 48.22 (95% UI 41.81–55.69) per 100,000. From 1990 to 2021, absolute numbers of prevalence, incidence, mortality, DALYs, YLLs, and YLDs increased by 43.56%, 44.82%, 10.68%, 11.02%, 7.64%, and 38.54%, respectively. Although the rates of prevalence and incidence showed slight increases of 0.07% and 0.96%, the rates of mortality, DALYs, YLLs, and YLDs decreased by 22.84%, 22.61%, 24.96%, and 3.42%, respectively. Among stroke subtypes, both ischemic stroke (IS) and intracerebral hemorrhage (ICH) showed increases in the absolute numbers across six metrics, with IS demonstrating more pronounced growth. Subarachnoid hemorrhage (SAH) showed increases in the incidence, prevalence, and YLDs, while its rates of mortality, DALYs, and YLLs declined. The rates of all six metrics decreased for ICH and SAH, whereas the rates of prevalence, incidence, and YLDs for IS increased, alongside reductions in the rates of mortality, DALYs, and YLLs. The absolute numbers and rates of all six metrics increased with age across both sexes, with males consistently showing higher absolute numbers and the highest burden observed in the 45-49 age group. Apart from the prevalence and YLD rates, males demonstrated higher incidence, mortality, DALYs, and YLL rates across all age groups, peaking at 45-49 years. Moreover, the leading contributors to stroke-related DALYs included high systolic blood pressure, smoking, and air pollution. From 2021 to 2050, the prevalence and incidence of stroke will continue to rise, while mortality and DALYs rates are expected to decline. Overall, from 1990 to 2021, the burden of stroke and its subtypes among young adults in Asia has increased significantly, with notable differences across age groups and sex, and with population growth and demographic changes, this burden is expected to further intensify in the future. Therefore, future research and public health policies should focus more on targeted interventions addressing the specific needs of young adults to effectively control and alleviate the burden of stroke.

To characterize patients with autoantibodies against metabotropic glutamate receptor 8 (mGluR8) and assess the pathogenicity of these antibodies. Anti-mGluR8 antibodies were detected via cell-based assay and immunoprecipitation. Clinical data from five anti-mGluR8-positive patients and previously reported cases with other anti-mGluR antibodies were reviewed. Patient-derived IgG was purified and absorbed using mGluR8-expressing or control HEK293T cells. Pathogenicity was tested in hippocampal neuron cultures and via passive transfer into mice, with ataxia evaluated using behavioral tests. Five patients (4 male, median age 61) presented with subacute ataxia; other symptoms included dysarthria, ophthalmoplegia, dysphagia, and cognitive changes. Brain MRI showed cerebellar and cortical atrophy in all cases. Immunotherapy led to transient improvement in all patients, with stabilization in three of four with follow-up. In vitro, non-mGluR8-absorbed IgG reduced synaptic mGluR8 clusters. Mice injected with non-mGluR8-absorbed IgG developed transient ataxia peaking at 3–6 h and resolving within 24 h, correlating with antibody binding to Purkinje cells. Anti-mGluR8 antibody is a novel possible biomarker for autoimmune ataxia, with its pathogenicity supported by passive transfer models.

BACKGROUND:Glial fibrillary acidic protein-immunoglobulin G (GFAP-IgG) positivity is associated with autoimmune GFAP astrocytopathy (GFAP-A), but also with other autoimmune encephalitides and viral infections. We attempted to elucidate the characteristics of GFAP-A in relation to other GFAP-IgG-positive encephalitides and constructed a differential diagnosis model. METHODS:141 GFAP-IgG-positive cases were identified, including 52 astrocytopathy (GFAP-A group), 48 autoimmune encephalitis (AE-G), and 41 viral encephalitis (VE-G). Multivariate logistic regression was employed to create a diagnostic model, with validation using an external cohort. RESULT:Compared to the AE-G group, the GFAP-A patients showed more onset age ≥ 50 years, headache, fever, consciousness disturbance, MRI radial vascular enhancement, cerebrospinal fluid (CSF) antibody titer grade ≥ 4, and CSF proteins ≥ 700 mg/L, but less female sex, limb numbness, visual disturbances, and CSF chloride ≤ 120 mmol/L. Among these, CSF antibody titer grade ≥ 4, CSF protein ≥ 700 mg/L, and absence of visual disturbances were independent risk factors for GFAP-A diagnosis. Compared to the VE-G group, the GFAP-A patients showed more course ≥ 14 days, onset age ≥ 50 years, limb weakness, serum potassium ≤ 3.9 mmol/L, CSF antibody titer grade ≥ 4, CSF leukocytes ≤ 46*10, MRI radial vascular enhancement, MRI involvement of brainstem, and MRI involvement of spinal cord, but less headache, fever, nausea, and vomiting. Among these, serum potassium ≤ 3.9 mmol/L, MRI spinal cord involvement, and absence of nausea and vomiting were independent risk factors for GFAP-A diagnosis. CONCLUSIONS:Based on critical clinical indicators identified, we constructed a differential diagnosis model for GFAP-A.

In clinical practice, we found cerebrospinal fluid magnesium concentration significantly lower in neuromyelitis optica spectrum disorder (NMOSD) patients compared to controls with non-autoimmune encephalitis neurological diseases. To investigate the effects and potential mechanisms of long-term magnesium supplementation on neuroinflammation, demyelination, and blood-brain barrier (BBB) integrity in NMOSD, we used two models: (1) NMOSD mouse model, which was induced by intraperitoneal injection of purified NMO-IgG to experimental autoimmune encephalomyelitis (EAE) mice, and (2) cultured human cerebral microvascular endothelial cells/D3 (hCMEC/D3). In the NMOSD mouse model, Magnesium L-threonate (MgT) pretreatment alleviated NMO-IgG-induced effects, including AQP4 loss, leukocyte infiltration, astrocyte and microglia activation, demyelination, decreased tight junction (TJ) protein expression, and neurological deficits. In vitro, MgT pretreatment ameliorated NMO-IgG induced damage to TJ protein expression in a (transient receptor potential melastatin 7) TRPM7-dependent manner. Magnesium supplementation shows potential protective effects against NMOSD, suggesting it may be a novel therapeutic approach for this condition. The beneficial effects appear to be mediated through preservation of blood-brain barrier integrity and reduction of neuroinflammation and demyelination.

OBJECTIVE:The objective of this study is to investigate the presence of astrocyte antibodies in patients, excluding aquaporin-4 or glial fibrillary acidic protein (GFAP) antibodies, while evaluating associated biomarkers and pathologies. METHODS:Patient serum and cerebrospinal fluid (CSF) were tested for antibodies using tissue- and cell-based assays. Neurofilament light chain (NFL) and GFAP in the CSF were detected using single-molecule array (SIMOA). RESULTS:116 patients accepted SIMOA. Fifteen functional neurological disorders patients without antibodies were designated as controls. Thirty-five patients were positive for astrocyte antibodies (Anti-GFAP: 7; Anti-AQP4: 7; unknown antibodies: 21, designed as the double-negative group, DNAP). The most frequent phenotype of DNAP was encephalitis (42.9%), followed by myelitis (23.8%), movement disorders (19.0%), and amyotrophic lateral sclerosis-like (ALS-like) disease (14.2%). The levels of CSF GFAP and NFL in DNAP were higher than in the control (GFAP: 1967.29 [776.60-13214.47] vs 475.38 [16.80-943.60] pg/mL, p < 0.001; NFL: 549.11 [162.08-2462.61] vs 214.18 [81.60-349.60] pg/mL, p = 0.002). GFAP levels decreased in DNAP (n = 5) after immunotherapy (2446.75 [1583.45-6277.33] vs 1380.46 [272.16-2005.80] pg/mL, p = 0.043), while there was no difference in NFL levels (2273.78 [162.08-2462.61] vs 890.42 [645.06-3168.06] pg/mL, p = 0.893). Two brain biopsy patterns were observed: one exhibited prominent tissue proliferation and hypertrophic astrocytes, with local loss of astrocytes, while the other showed severe astrocyte depletion with loss of neurofilaments around the vessels. Eighteen patients received immunotherapy, and improved except one with ALS-like symptoms. We identified anti-vimentin in this patient. DISCUSSION:There are unidentified astrocyte antibodies. The manifestations of double-negativity are heterogeneous; nevertheless, the pathology and biomarkers remain consistent with astrocytopathy. Immunotherapy is effective.

Background: In clinical practice, autoimmune glial fibrillary acidic protein astrocytopathy (GFAP-A) and tuberculous meningitis (TBM) are difficult to discriminate. Many GFAP-A patients have been misdiagnosed as TBM and have been unnecessarily administered antituberculosis therapy. This study aimed to establish a diagnostic model that could distinguish between GFAP-A and TBM.Methods: We conducted an observational study on multi-center clinical data from 396 GFAP-A and 73 TBM control patients. We randomly divided our dataset into validation and training sets. We used both univariate and multivariate logistic regression to develop a model for disease discrimination.Findings: In Cohort A, 91 of 396 GFAP-A patients were identified as possible TBM cases. Of these 91 patients, 25 accepted antituberculosis therapy before immunotherapy, but only 2 of these 25 patients were confirmed to be TBM cases. The remaining patients did not accept antituberculosis therapy, with one of them confirmed to be TBM. In Cohort B, 19 of 73 TBM patients tested positive on tissue-based assay (TBA). Of these 19 patients, 11 presented other autoantibodies and 8 were positive for GFAP-IgG. Compared with TBM, GFAP-A presented more focal neurological deficits except cranial nerve palsies, lower multinuclear cell proportion, higher lymphocyte proportion in cerebrospinal fluid (CSF), more longitudinal radial perivascular enhancement, more spinal cord lesion on MRI, and higher viral content in the CSF as recorded by next-generation sequencing (NGS). Three characteristics were predictive of a diagnosis of GFAP-A: lymphocyte proportion in CSF≥80%, viral presence in CSF detected by NGS, and focal neurological deficits excluding cranial nerve palsies. We validated the model on both internal and external datasets.Interpretation: Our diagnostic model, which is based on the combination of three relevant indicators, helps differentiating between GFAP-A and TBM with or without GFAP-IgG. Following further validation by future prospective studies, it may guide treatment decisions in the clinic.Funding: This study was supported by the National Natural Science Foundation of China (81771302), Multi-center Project of The Second Affiliated Hospital of Guangzhou Medical University (2020-LCYJ-XJS-03, 2022-LCYJ-YYDZX-04) and the Wisdom Accumulation and Talent Cultivation Project of the Third Xiangya Hospital of Central South University (YX202205).Declaration of Interest: The authors declare that no competing interests exist.Ethical Approval: The study protocol (No. 2022-hs-56-02, 2020-hs-54) was approved by the Ethics Committee of the Second Affiliated Hospital of Guangzhou Medical University (Guangzhou China). Participants gave informed consent to participate in the study before taking part.

To explore the autoimmune response and outcome in the central nervous system (CNS) at the onset of viral infection and correlation between autoantibodies and viruses. Methods A retrospective observational study was conducted in 121 patients (2016–2021) with a CNS viral infection confirmed via cerebrospinal fluid (CSF) next-generation sequencing (cohort A). Their clinical information was analysed and CSF samples were screened for autoantibodies against monkey cerebellum by tissue-based assay. In situ hybridisation was used to detect Epstein-Barr virus (EBV) in brain tissue of 8 patients with glial fibrillar acidic protein (GFAP)-IgG and nasopharyngeal carcinoma tissue of 2 patients with GFAP-IgG as control (cohort B). Results Among cohort A (male:female=79:42; median age: 42 (14–78) years old), 61 (50.4%) participants had detectable autoantibodies in CSF. Compared with other viruses, EBV increased the odds of having GFAP-IgG (OR 18.22, 95% CI 6.54 to 50.77, p<0.001). In cohort B, EBV was found in the brain tissue from two of eight (25.0%) patients with GFAP-IgG. Autoantibody-positive patients had a higher CSF protein level (median: 1126.00 (281.00–5352.00) vs 700.00 (76.70–2899.00), p<0.001), lower CSF chloride level (mean: 119.80±6.24 vs 122.84±5.26, p=0.005), lower ratios of CSF-glucose/serum-glucose (median: 0.50[0.13-0.94] vs 0.60[0.26-1.23], p =0.003), more meningitis (26/61 (42.6%) vs 12/60 (20.0%), p=0.007) and higher follow-up modified Rankin Scale scores (1 (0–6) vs 0 (0–3), p=0.037) compared with antibody-negative patients. A Kaplan-Meier analysis revealed that autoantibody-positive patients experienced significantly worse outcomes (p=0.031). Conclusions Autoimmune responses are found at the onset of viral encephalitis. EBV in the CNS increases the risk for autoimmunity to GFAP.

BACKGROUND AND OBJECTIVES:Brain radial enhancement pattern on magnetic resonance imaging (MRI) has been identified as typical lesions in autoimmune glial fibrillary acidic protein astrocytopathy (GFAP-A). However, the authors encountered several patients without GFAP-IgG showing that such specific imaging. In the present study, we reported the clinical pictures of 5 GFAP-IgG-negative patients with GFAP-A specific imaging pattern.METHODS:Data was retrospectively obtained from June 2013 through April 2023, and five GFAP-IgG-negative patients with valid data were recruited. Clinical information was either obtained by the investigators or retrieved from the referring clinicians and included prodromal symptoms, neurologic manifestations, comorbidities, results of ancillary studies.RESULTS:Altogether five GFAP-IgG-negative patients with "meningoencephalitis/encephalitis" manifestations and brain radial perivascular enhancement were confirmed. One patient had peripheral lymphoma. Four patients had other autoimmune antibody in serum and/or cerebrospinal fluid, of which one patient had positive aquaporin IgG. Clinical features of the five patients included headache, fever, epilepsy and abnormal behavioral symptoms. MRI of patients revealed radial perivascular gadolinium enhancement extending from the lateral ventricles to the white matter suggestive of autoimmune GFAP-A.CONCLUSION:GFAP-A-like disorders with radial perivascular enhancement could be found in GFAP-IgG-negative patients with or without neoplasm, which could provide new insight into the differential diagnosis of GFAP-A.

Background: Neuromyelitis optica spectrum disorder (NMOSD) is a rare and severe inflammatory demyelinating disorder of the central nervous system (CNS), which mainly affects the optic nerves and spinal cord. The aims of this study were to determine whether the expression levels of serological cytokines could distinguish 1) NMOSD from healthy controls (HCs); and 2) NMOSD patients with and without the aquaporin-4 (AQP4) antibody biomarker from each other; and 3) NMOSD patients without the antibody to AQP4 from MS patients.Methods: The expression levels of 200 proteins in serum from 41 NMOSD (32 with antibodies to AQP4, 9 without antibodies to AQP4), 12 MS patients, and 34 HCs were measured using glass-based antibody arrays. None of the patients received any immunosuppressive treatment. In parallel, the correlation between protein expression in NMOSD/MS patients and clinical traits was determined with Weighted Gene Co-expression Network Analysis (WGCNA).Results: Thirty-nine serological proteins were differentially expressed in NMOSD patients compared to HCs, with 29 of these proteins not observed in MS patients. In addition, the data reveal 15 differentially-expression proteins (DEPs) between AQP4-IgG seronegative and AQP4-IgG seropositive NMOSD patients, and 9 DEPs between NMOSD and MS patients who did not have AQP4-IgG.Conclusion: Serological IL-17B is significantly upregulated in both NMOSD and MS patients compared to HCs, and could be a key biomarker of NMOSD and MS. Serological VEGF, MPIF-1 and NrCAM were positively associated with AQP4-IgG titer. We also demonstrate that EGF may be involved in the breakdown of the BBB by down regulating Claudin-5.

目的 探讨自身免疫性胶质纤维酸性蛋白星形细胞病的脑膜脊膜病变特点,旨在提高临床医师对自身免疫性胶质纤维酸性蛋白星形细胞病(GFAP-A)的认识与诊治.方法 一项回顾性病例对照研究.通过免疫荧光的方法检测出阳性的GFAP-IgG 55例,其中28例患者完成头颅MRI的平扫和增强(25例同时完成脊髓MRI平扫和增强).对照组为同期住院的27例AQP4-IgG阳性的视神经脊髓炎谱系疾病患者,均完成头颅和脊髓MRI平扫和增强.结果 纳入28例GFAP-A,主要临床症状包括头痛(46.4％,13/28)、发热(57.1％,16/28)、脊髓炎(42.9％,12/28)、视觉异常(39.3％,11/28)、行为异常(28.6％,8/28)、共济失调(25.0％,7/28)、意识障碍(14.3％,4/28)、癫痫发作(10.7％,3/28)、运动障碍(7.1％,2/28)、认知障碍(10.7％,3/28)和其他症状(25％,7/28).MRI增强下15例(53.6％)出现脑膜和(或)脊膜的异常信号,其中脑膜异常8例(28.6％),脊膜异常3例(10.7％),脑膜与脊膜同时异常4例(14.3％).两例病理资料显示脑膜增厚,慢性炎症改变.与视神经脊髓炎谱系疾病对比显示性别比例、发热、头痛、行为异常、视觉异常、MRI放射性血管样强化、脊髓异常、长节段脊髓炎、脑膜和(或)脊膜异常差异均有统计学意义(P<0.05).

Abstract ObjectiveThe aims of this study were to determine whether the expression levels of serological cytokines could distinguish 1) neuromyelitis optical spectrum disorders (NMOSD) from healthy controls (HCs); and 2) NMOSD patients with and without the aquaporin-4 (AQP-4) antibody biomarker from each other; and 3) NMOSD patients without antibody to AQP-4 from multiple sclerosis (MS). MethodsThe expression levels of 200 proteins in serum from 41 NMOSD (32 with antibodies to AQP-4, 9 without antibodies to AQP-4), 12 MS patients, and 34 HCs were measured using glass-based antibody arrays. In parallel, the correlation between protein expression in NMOSD/MS patients and clinical traits was analyzed with Weighted Gene Co-expression Network Analysis (WGCNA).ResultsThirty-nine serological proteins were differentially expressed in NMOSD patients compared to HCs. 29 differentially-expression proteins (DEPs) were specific to NMOSD whereas 10 of these were observed in NMOSD and MS samples. In addition, there were 15 DEPs between AQP-4-IgG seronegative and AQP-4-IgG seropositive NMOSD patients, and 9 DEPs between NMOSD and MS patients who did not have AQP-4-IgG. ConclusionsOur findings highlight that serological Interleukin-17B (IL-17B) may be key biomarker of NMOSD and MS. While epidermal growth factor (EGF) may be correlated with the breakdown of the blood-brain barrier in NMOSD patients, granulocyte chemotactic protein-2 (GCP-2) and monocyte differentiation antigen CD14 (CD14) may play different roles in the pathogenesis of AQP-4-IgG seronegative and seropositive NMOSD and MS. Novel biomarkers identified in our study could potentially be used in the diagnosis and treatment of NMOSD.Trial registrationPublic title: Multi-Center Clinical Study of GFAP AstrocytopathyRegistration number: ChiCTR2000041291Date of registration: 2020-12-23 (Retrospective registration)URL of trail registry record: http://www.chictr.org.cn/showproj.aspx?proj=65306

目的 探讨自身免疫性GFAP星型细胞病的脑电图(electroencephalographic,EEG)的特点.方法 对确诊自身免疫性GFAP星型细胞病患者的临床和脑电图等资料进行回顾性分析.分析不同临床表现患者脑电图、头MR影像特点,随访3～12个月.结果 共纳入自身免疫性GFAP星型细胞病患者38例,主要临床表现包括肢体乏力、麻木(n=20,52.6％)、发热(n=14,42.1％)、头痛(n=16,42.1％)、排便障碍(n=9,23.7％)、癫痫发作(n=5,13.2％).26例患者有效脑电图记录中3例可见各导联弥漫性慢活动出现,5例出现癫痫样放电,9例出现散在慢波,9例正常脑电图.结论 EEG对自身免疫性GFAP星型细胞病的诊断、追踪随访及预后评估有实用意义.

神经内科是临床医学专业里重要的二级学科,很多非神经内科的规培医生需要到神经内科轮转.目前各教学医院神经内科轮科医生的教学和培养方案存在差异,培养和教学质量参差不齐.为了提高神经内科轮科医生的教学和培养质量,该文根据该中心的教学经验,针对如何提高神经内科轮科医生的培养和教学质量,就常见疾病的教学、科室核心制度的教学、病历文书书写与修改教学、因专业而制宜的学科结合式教学、病例分析及临床思维教学、常用药物及抢救药物的教学、医患沟通能力和技巧的教学等方面进行系列阐述,以期给同行提供经验参考.

Objective To analyze the magnetic resonance imaging (MRI) of the spinal cord and clinical characteristics in patients with autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy.Methods A total of 1 040 samples of cerebrospinal fluid (CSF) and sera collected in the Second Affiliated Hospital of Guangzhou Medical University from March 2013 to June 2018 were tested with tissue-and cell-based assays,and 42 patients were found positive for GFAP-IgG.The clinical data and MRI characteristics of the spinal cord of 19 patients who were positive for GFAP-IgG in CSF with autoimmune GFAP astrocytopathy and lesions in the spinal cord were retrospectively reviewed.Results There were 12 females and seven males among the 19 patients,with onset age of (44±17) years.The main manifestations of these patients included limb weakness (14/19),abnormal vision (5/19),headache (4/19),seizure (4/19),dementia (3/19),etc.On MRI of the spinal cord,five patients showed involvement in the cervical cord alone,eight showed involvement in the thoracic cord alone and six had both cervical and thoracic segment involvement.Fifteen patients had longitudinally extensive myelitic abnormalities (≥3 vertebral segments long).Seven enhancement patterns were encountered.Lesions were displayed in the spinal cord and brain in eight patients.Central gray matter involvement in the spinal cord was found in all the 19 patients.Conclusions Autoimmune GFAP astrocytopathy more frequently presents in females than in males.MRI of the spinal cord has complex presentations and longitudinally extensive myelitic abnormalities usually.Patients often show central gray matter involvement in the spinal cord.Myelitic abnormalities present more often in thoracic segment than in cervical segment.Abnormalities in lumbar segment are less encountered.

BACKGROUND:In this study, we describe clinical findings in a patient with autoimmune inflammatory meningoencephalitis who was negative for antibodies against glial fibrillary acidic protein (GFAP-IgG).METHODS:Serum and cerebral spinal fluid (CSF) samples were collected from the patient as part of a study of 520 patients with neurological syndromes. Antibodies against GFAP and other proteins associated with neurological disorders were measured by rat brain- and cell-based indirect immunofluorescence assays.RESULTS:A 42-year-old female was diagnosed with autoimmune inflammatory meningoencephalitis. She experienced a subacute and relapsing course with decreased vision, fever, headache, ataxia, hemiplegia, and disturbance of consciousness. Brain magnetic resonance imaging showed extensive lesions in the white matter along the ventricle, brainstem, right internal capsule, and meninges. The patient responded well to steroid treatment. Examination of CSF revealed a normal white blood cell count and protein level. Serum and CSF were negative for GFAP-specific antibodies and all other autoantibodies tested. Immunohistochemical staining of a brain biopsy collected during relapse revealed chronic inflammation and severe edema. Extensive and strong staining of CD163+ macrophages were evident throughout the lesions; however, CD3+ cells were rare and CD138+ and CD20+ cells were absent.CONCLUSION:We describe a case of subacute corticosteroid-responsive nonvasculitic autoimmune inflammatory meningoencephalitis in the absence of GFAP-IgG. The pathological features were distinct from those of patients with GFAP-IgG-positive meningoencephalitis, suggesting that nonvasculitic autoimmune inflammatory meningoencephalitis is a heterogeneous neurological syndrome.

Aim: To investigate the clinical features of five glial fibrillary acidic protein (GFAP) antibody positive patients with suspected benign tumors and explore its underlying pathogenesis. Materials and methods: Overall, 1018 serum and cerebrospinal fluid (CSF) samples were tested by indirect immunofluorescence assay and data from five patients with suspected tumors and positive for GFAP autoantibody in the CSF were analyzed retrospectively. Results: The positive rate of GFAP antibody in the serum and CSF was 3.93% by indirect immunofluorescence assay. Tumors were diagnosed before or after neurologic onset in 5 of 40 patients (12.5%) and no deterioration of the tumors was found during the long-term follow-up. Of the five patients, one patient suffered a thyroid nodule, one patient had a small nodule in the left lung, two patients suffered meningiomas, and one patient had a suspicious eosinophilic granuloma. Conclusion: GFAP autoimmunity may be a paraneoplastic immune response with a low frequency of tumor in Chinese patients with GFAP astrocytopathy.

Objective: Determination of glial fibrillary acidic protein (GFAP), aquaporin 4 (AQP4), and myelin oligodendrocyte glycoprotein (MOG) levels in cerebrospinal fluid (CSF), and astrocytic damage analysis in patients with GFAP astrocytopathy (GFAP-A) and other conditions. Methods: GFAP, AQP4, and MOG levels in CSF were detected via enzyme-linked immunosorbent assays. Anti-GFAP, anti-AQP4, and anti-MOG IgGs were detected via indirect immunofluorescence assays. Results: In 32 GFAP-Astrocytopathy patients, CSF GFAP was significantly higher during acute exacerbation than it was in patients with MOG encephalomyelitis, multiple sclerosis, autoimmune encephalitis, and an "other inflammatory neurological disorders" group (all p < 0.0001). CSF GFAP levels were slightly higher in the GFAP-A group than in an anti-AQP4 IgG-positive neuromyelitis optica spectrum disorder group (p = 0.012). There were no significant differences between the CSF MOG and AQP4 levels in the GFAP-A group and those of other groups. CSF GFAP levels were significantly reduced after steroid treatment (p = 0.011). CSF GFAP levels differed significantly in GFAP-Astrocytopathy patients with and without encephalitis (p = 0.016). In GFAP-Astrocytopathy patients, CSF GFAP was correlated with Expanded Disability Status Scale (EDSS) score during attack (r = 0.545, p = 0.001). In follow-up examinations however, in GFAP-Astrocytopathy patients CSF GFAP level was not correlated with EDSS score 6 months later. Conclusions: CSF GFAP level and pathological examination of GFAP-Astrocytopathy patients revealed astrocyte damage. CSF GFAP level was associated with steroid treatment at the acute stage, therefore CSF GFAP may be a sensitive biomarker with respect to the effects of therapy during the acute stage.

Objective To analyze the risk factors,pathogeny,differential diagnosis and treatment protocols of transient global amne-sia. Methods Clinical data of 15 cases of clinically diagnosed transient global amnesia were collected,and the symptoms,risk fac-tors,auxiliary examinations,differential diagnosis and treatment protocols were analyzed. Results The auxiliary examination results showed that the cerebral vessels of 15 cases of transient global amnesia were ischemic. The treatment protocols of improving circulation, repairing nerves and antiplatelet therapy were effective,and no recurrence was found. Conclusion Transient global amnesia is likely to be associated with cerebral ischemia. The treatment protocols of ischemic cerebrovascular disease can achieve good results and effec-tively prevent the recurrence of the disease.

Objective: The aim of this study was to evaluate the positive rate of serum glutamic acid decarboxylase (GAD) autoantibody in patients with myelitis and to describe the clinical findings in patients with positive GAD antibody. Methods: Serum samples were collected from 390 patients with myelitis, including 210 patients positive for aquaporin 4 (AQP4) antibody and 180 patients negative for AQP4. GAD65 antibody was measured by an indirect immunofluorescence assay. Results: Only 1 serum and cerebral spinal fluid sample from 390 patients (0.26%) was positive for anti-GAD antibodies. The patient was a female with relapsing myelitis and a thymic mass. Thymic resection was undertaken, and pathological examination revealed a benign thymic cyst. Extensive infiltration of lymphocytes positive for CD3, CD4, CD8 and CD20 was found. Immunohistochemistry showed positive expression of GAD65 in the cyst. Conclusions: Although serum GAD65 antibodies were present in a patient, it is not recommended to routinely screen for GAD65 antibodies in patients with myelitis because of their rare occurrence. However, screening for GAD65 antibodies should be considered in patients who have been diagnosed with cancer or a thymic abnormality.