Effects of Transcranial Direct Current Stimulation on Clinical Outcomes, Calcitonin Gene-Related Peptide, and Pituitary Adenylate Cyclase-Activating Polypeptide-38 Levels in Menstrual Migraine.

OBJECTIVES: Transcranial direct current stimulation (tDCS) has been suggested as an alternative treatment option for migraine. The present study aimed to evaluate the efficacy of tDCS on clinical outcomes in addition to calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase-activating peptide 38 (PACAP-38) levels in individuals with menstrual-related migraine (MRM) for the first time. MATERIALS AND METHODS: In this parallel study, 58 female patients between the ages of 18 and 45 years, including 36 with MRM and 22 with nonmenstrual migraines (nMM), were recruited. Sessions of 2-mA 20-minute anodal tDCS were administered over the left dorsolateral prefrontal cortex within three consecutive days (1:1 active and sham stimulation). Migraine attack frequency, severity, analgesic usage, CGRP, and PACAP-38 levels of the patients were evaluated before and one month after tDCS. RESULTS: After tDCS, in the active group compared with the sham group, the frequency (p = 0.031), the severity of attacks (p = 0.003), the number of days with headache (p = 0.004), and the analgesic usage (p = 0.024) were all decreased. In both MRM and nMM groups, the frequency and severity of attacks and analgesic usage were decreased in those receiving active stimulation (p < 0.001 for each). CGRP and PACAP-38 levels were no different in the active group and the sham group after tDCS. CONCLUSIONS: tDCS was shown to be efficacious in migraine prophylaxis and a valuable option for migraine and MRM treatment. The absence of changes in serum CGRP and PACAP-38 levels suggests that tDCS efficacy may stem from distinct cerebral electrophysiological mechanisms.

Investigation of the effects of oxidative stress, inflammation on the pathway of tryptophan/kynurenine in OCD.

OBJECTIVES: Recent studies have shown that the distribution of the tryptophan/kynurenine pathway (KP) plays a role in the development of obsessive-compulsive disorder (OCD). We aimed to reveal the relationship between CYP1A1 rs464903 and aryl hydrocarbon receptor (AhR) rs10249788 associated with the KP and interferon gamma (IFN γ) and oxidative stress in OCD. METHODS: In our study, the serum and DNAs of 150 samples, including 100 OCD patients and 50 controls, were used. The activity of glutathione peroxidase (GSH-Px), and the levels of IFN γ, thiobarbituric acid reactive substances (TBARS), tryptophan, and kynurenine were determined by biochemical methods. AhR rs10249788 and cytochrome P450 family CYP1A1 rs4646903, which interact directly with the KP, were analysed by polymerase chain reaction followed by restriction fragment length polymorphism. P < 0.05 was considered statistically significant. RESULT: There were no significant differences between groups in CYP1A1 rs4646903 and AhR rs10249788 while tryptophan and IFN γ were found to be higher in controls (p < 0.001, for both), and TBARS and indolamine-2,3-dioxygenase were found to be higher in OCD (p < 0.001, for both). There were significant correlations between IFN γ and TBARS and GSH-Px (p = 0.028, p = 0.020, respectively) in the OCD group. CONCLUSIONS: For the first time studied in OCD, it has been shown that IFN γ, tryptophan, oxidative stress parameters, and gene variants of CYP1A1 rs4646903 anAhR rs10249788 are shown effective on the KP.

Reduced expression of inflammasome complex components in cluster headache.

BACKGROUND: The involvement of inflammation in the pathophysiology of cluster headache (CH) has been suggested, with a role implied for interleukin (IL)-1ß. We aimed to measure peripheral blood expression levels of IL-1ß-inducing systems, the inflammasome complex, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling, and investigate their values as putative biomarkers in CH. METHODS: In this cross-sectional study conducted in the Headache Unit of Istanbul University, Turkey, blood mononuclear cells (PBMCs) and sera were collected from 30 patients with episodic migraine, 4 with chronic CH, and 47 healthy individuals. Levels of inflammasome complex components (NLRP1, NLRP3, caspase 1, and ASC), end products of inflammasome complex activity (IL-1ß, IL-18, and nitric oxide synthase isoforms), neuron-specific enolase, other inflammatory factors (NF-κB, HMGB1, and s100b), and anti-inflammatory IL-4 were measured by real-time quantitative polymerase chain reaction and/or enzyme-linked immunosorbent assay. RESULTS: NLRP3 expression levels were significantly reduced in PBMC samples of patients with CH, obtained during CH attacks (n = 24) or headache-free (out of cycle) episodes (n = 10). CH-attack patients showed greater expression levels of IL-1ß (2-ΔΔCT median [25th-75th percentile], 0.96 [0.66-1.29 vs. 0.52 [0.43-0.73]) and NF-κB (1.06 [0.66-3.00] vs. 0.62 [0.43-1.19]) in PBMCs but not in sera compared with headache-free CH patients. However, these differences did not attain statistical significance (p = 0.058 and p = 0.072, respectively). Moreover, NLRP1 (52.52 [35.48-67.91] vs. 78.66 [54.92-213.25]; p = 0.017), HMGB1 (11.51 [5.20-15.50] vs. 13.33 [8.08-18.13]; p = 0.038), S100b (569.90 [524.10-783.80] vs. 763.40 [590.15-2713.00]; p = 0.013), NSE (11.15 [6.26-14.91] vs. 13.93 [10.82-19.04]; p = 0.021), nNOS (4.24 [3.34-12.85] vs. 12.82 [4.52-15.44]; p = 0.028), and eNOS (64.83 [54.59-91.14] vs. 89.42 [61.19-228.40]; p = 0.034) levels were lower in patients with three or more autonomic manifestations (n = 9). No correlation was found between inflammation factors and clinical parameters of CH. CONCLUSION: Our results support the involvement of the IL-1ß system in attacks of CH. However, the components of the inflammasome complex are suppressed in the peripheral blood and do not appear to play a role in the pathophysiology of CH. These findings argue against a potential biomarker value of the inflammasome complex in CH.

Cerebrospinal fluid level of neurofilament light chain is associated with increased disease activity in neuro-Behçet's disease.

BACKGROUND: Clinical exacerbations characterized with neurological symptoms are observed in around 10% of Behçet's disease (BD) patients and may culminate in severe disability. Although certain immunological factors have been associated with disease activity in neuro-Behçet's disease (NBD), biomarkers for monitoring the clinical outcome of NBD have not been properly investigated. METHODS: Levels of neurofilament light chain (NFL), homeobox protein Hox-B3 (HoxB3), and YKL-40 were measured in cerebrospinal fluid (CSF) samples of 23 parenchymal (n = 16) and nonparenchymal (n = 7) NBD patients obtained during NBD attacks by ELISA. Parameters of clinical progression and outcome were assessed for an average follow-up period of 3.9 ± 1.3 years. RESULTS: Parenchymal NBD patients showed elevated CSF levels of NFL, HoxB3, and YKL-40 as compared to nonparenchymal patients. NBD patients showing an increase in modified Rankin score (mRS) values during follow-up had significantly higher CSF NFL levels. Patients with relatively lower CSF NFL levels (<1000 ng/L) did not develop attacks or cognitive impairment interfering with daily life activities during follow-up. NFL levels correlated with disease duration and mRS at the last follow-up visit, while HoxB3 levels correlated with a number of attacks during follow-up. DISCUSSION: CSF level of NFL appears to predict the prospective somatic and cognitive disability in NBD patients and may thus be potentially used as a biomarker of clinical outcome in this disease.

Plasma levels of inflammatory mediators in vestibular migraine.

Objectives: Vestibular migraine (VM) is an under-recognized entity with substantial burden for the individual and society. The underlying mechanism of VM and its distinction from other migraine mechanisms still remain unclear. Inflammatory pathways have been suggested to contribute to vestibular migraine. Our aim was to further investigate the possible role of inflammation in the pathophysiology of VM.Methods: We recruited 30 patients with VM diagnosed according to ICHD-3 criteria and 50 gender- and age-matched controls. Blood samples were obtained from 11 VM patients during an attack and from 13 VM patients under prophylactic treatment. Plasma levels of calcitonin gene related peptide (CGRP), neurokinin A (NKA), substance P (SP), NLRP1, NLRP3, caspase-1, IL-1ß, IL-6, TNF-α and NFκB were measured by ELISA.Results: IL-6 levels were significantly reduced in VM patients, whereas levels of other inflammation parameters were comparable to those of healthy controls. Levels of inflammatory mediators were not correlated with clinical parameters. Likewise, there were no significant differences among VM patients with and without headache attack and prophylactic treatment.Conclusion: Our results argue against involvement of systemic inflammation in the pathophysiology of VM.

Video-Oculography Assessment in Neurodegenerative Ataxias and Niemann Pick Type C.

Introduction: Deceleration of vertical saccades, an early and characteristic finding of Niemann-Pick Type C (NP-C), may help diagnosis. Our aim in this study was to demonstrate the role of video-oculography (VOG), in the differential diagnosis of ataxia syndromes, particularly of NP-C, using this technique in the evaluation of saccadic velocity and smooth pursuit gain of ataxia patients. Methods: We recruited consecutive 50 ataxia patients and 50 healthy control subjects who were age and sex-matched with the patient group. Saccadic eye movements and smooth pursuit eye movements for different angles and different directions from patients and healthy subjects were recorded by using VOG. Results: Saccadic eye movement velocity and smooth pursuit gain values of the patients were significantly lower in all directions and at all angles as compared to healthy subjects. In the patient group, 3 cases out of 50 were selected as suspected NP-C, based on the dissociation between their markedly impaired vertical saccadic velocity and near normal to slightly impaired horizontal one and relatively intact smooth pursuit eye movements; the diagnoses in all 3 cases were confirmed with positive genetic testing, and thereupon Miglustat treatment was started. Conclusion: Our findings support that cerebellar pathology in degenerative ataxia patients is associated with both impaired saccadic velocity and smooth pursuit gain, whereas in NP-C, only the impaired vertical saccades as opposed to relatively preserved other eye movements are seemingly a diagnostic marker for the entity. We conclude that recording of eye movements could be useful for differential diagnosis and monitorization of the treatment of ataxia syndromes as an easy and objective method.

The Prevalence of Headache Disorders in Children and Adolescents in Istanbul: A School-Based Study.

BACKGROUND: Headache among children and adolescents is an important health problem. In this school-based epidemiological study conducted in Istanbul, we aimed to reveal the frequency of headaches in this population, define the risk factors associated with headaches, and establish the effect of headaches on the quality of life in this population. METHODS: The child and adolescent versions of the Headache-Attributed Restriction, Disability, Social Handicap and Impaired Participation structured questionnaire were conducted in 30 schools in Istanbul. The diagnosis was made based on the International Classification of Headache Disorders III-(ICHD-3) beta version. Risk factors associated with headaches were analyzed in a binary logistic regression model. RESULTS: Among the 5944 students (boys = 3011 [50.7%], girls 2933 [49.3%]) who completed the survey and were enrolled in this study, 3354 (56.4%) reported a headache ever. The prevalence of headaches was significantly higher in girls (62.6% vs. 50.4%, P < 0.001). Migraine prevalence was found to be 5.2%, whereas tension-type headache (TTH) prevalence was 26.1%. Being a female, age, living on the European side, and headache history in the family were found to be associated with an increased risk of having a headache. Pupils with headaches reported that they missed an average of 0.5 ± 1.5 school days due to headaches. CONCLUSION: TTH was found to be the most common headache syndrome in Istanbul metropolitan area. Considering the effect of headaches on school success and quality of life in childhood, it is clear that the correct diagnosis of headaches and careful handling of risk factors are crucial for this population.

Serum CXCL5 as a biomarker in multiple sclerosis and neuromyelitis optica spectrum disorder.

OBJECTIVE: Our aim was to determine whether serum C-X-C motif chemokine 5 (CXCL5) may serve as a diagnostic biomarker for relapsing-remitting multiple sclerosis (RRMS) as well as a marker that can be used to predict treatment response. METHODS: CXCL5 levels were measured by ELISA in sera of 20 RRMS patients under fingolimod treatment, 10 neuromyelitis optica spectrum disorder (NMOSD) patients, 15 RRMS patients presenting predominantly with spinal cord and optic nerve attacks (MS-SCON), and 14 healthy controls. RESULTS: Fingolimod treatment significantly reduced CXCL5 levels. CXCL5 levels were comparable among NMOSD and MS-SCON patients. CONCLUSION: Fingolimod might regulate the innate immune system. Serum CXCL5 measurement does not differentiate between RRMS and NMOSD.

Chloride intracellular channel protein-1 (CLIC1) antibody in multiple sclerosis patients with predominant optic nerve and spinal cord involvement.

INTRODUCTION: Antibodies to cell surface proteins of astrocytes have been described in chronic inflammatory demyelinating disorders (CIDD) of the central nervous system including multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). Our aim was to identify novel anti-astrocyte autoantibodies in relapsing remitting MS (RRMS) patients presenting predominantly with spinal cord and optic nerve attacks (MS-SCON). METHODS: Sera of 29 MS-SCON patients and 36 healthy controls were screened with indirect immunofluorescence to identify IgG reacting with human astrocyte cultures. Putative target autoantigens were investigated with immunoprecipitation (IP) and liquid chromatography-mass/mass spectrometry (LC-MS/MS) studies using cultured human astrocytes. Validation of LC-MS/MS results was carried out by IP and ELISA. RESULTS: Antibodies to astrocytic cell surface antigens were detected in 5 MS-SCON patients by immunocytochemistry. LC-MS/MS analysis identified chloride intracellular channel protein-1 (CLIC1) as the single common membrane antigen in 2 patients with MS-SCON. IP experiments performed with the commercial CLIC1 antibody confirmed CLIC1-antibody. Home made ELISA using recombinant CLIC1 protein as the target antigen identified CLIC1 antibodies in 9/29 MS-SCON and 3/15 relapsing inflammatory optic neuritis (RION) patients but in none of the 30 NMOSD patients, 36 RRMS patients with only one or no myelitis/optic neuritis attacks and 36 healthy controls. Patients with CLIC1-antibodies showed trends towards exhibiting reduced disability scores. CONCLUSION: CLIC1-antibody was identified for the first time in MS and RION patients, confirming once again anti-astrocytic autoimmunity in CIDD. CLIC1-antibody may potentially be utilized as a diagnostic biomarker for differentiation of MS from NMOSD.

Is Video-Oculography a Predictive Test for Myasthenia Gravis with Ocular Symptoms?

Background and Objective: The aim of this study was to evaluate the contribution of extraocular muscle function testing with video-oculography (VOG), which is a noninvasive and easily applicable method of recording eye movement with digital cameras, to the diagnosis of myasthenia gravis (MG) in patients without any clinical eye movement abnormalities. Methods and Materials: The study included 18 patients prediagnosed with ocular MG: MG Group (N = 7) with abnormal, and non-MG Group (N = 11) with normal single-fiber electromyography. Control group included 50 healthy volunteers. Ocular movements were recorded with the EyeSeeCam VOG device. Results: The inward latency of the 10° horizontal saccade and the downward latency of the 10° vertical saccade were significantly delayed; and the downward amplitude of the 10° vertical saccade was significantly lower in the MG group. Receiver operating characteristic curve analyses showed high specificity values for the discrimination of MG patients. Conclusions: This study supports the usefulness of the VOG device in revealing subclinical extraocular muscle involvement in MG.

Kv5.1 antibody in epilepsy patients with unknown etiology.

BACKGROUND: Neuronal autoantibodies and favorable response to immunosuppressive treatment have been described in patients with chronic epilepsy of unknown cause, suggesting autoimmune etiology. Our aim was to identify novel epilepsy-specific autoantibodies reactive with neuronal surface antigens. METHODS: Sera of 172 epilepsy patients with unknown cause and 30 healthy controls were screened with indirect immunofluorescence to identify IgG reacting with primary rat neuronal cultures. Putative target autoantigens were investigated with immunoprecipitation (IP) and liquid chromatography-mass/mass spectrometry (LC-MS/MS) studies using SH-SY5Y cells. Validation of LC-MS/MS results was carried out by IP and immunocytochemistry assays. RESULTS: Antibodies to neuronal cell surface antigens were detected in 18 epilepsy patients. LC-MS/MS analysis identified voltage-gated potassium channel modifier subfamily F member 1 (KCNF1, Kv5.1) as the single common cell surface antigen in 4 patients with Lennox-Gastaut syndrome (n = 2), focal epilepsy of unknown cause (n = 1) and mesial temporal lobe epilepsy with hippocampal sclerosis (n = 1). These patients had the common features of early seizure onset and treatment-resistance. IP assays and co-localization (serum IgG and commercial Kv5.1-antibody) studies done with non-fixed Kv5.1-transfected HEK293 cells and primary neuronal cultures confirmed the presence of Kv5.1-antibody in 4 epilepsy patients identified by LC-MS/MS. Similar findings were not obtained by sera of other patients with epilepsy, patients with autoimmune encephalitis and healthy controls. CONCLUSION: The herein described novel neuronal surface antibody to Kv5.1 appears to be associated with treatment-resistant epilepsy of unknown cause. Exact clinical and pathogenic significance of this antibody remains to be elucidated.

Inflammation and regulatory T cell genes are differentially expressed in peripheral blood mononuclear cells of Parkinson's disease patients.

Our aim was to identify the differentially expressed genes (DEGs) in peripheral blood mononuclear cells (PBMC) of Parkinson's disease (PD) patients and healthy controls by microarray technology and analysis of related molecular pathways by functional annotation. Thirty PD patients and 30 controls were enrolled. Agilent Human 8X60 K Oligo Microarray was used for gene level expression identification. Gene ontology and pathway enrichment analyses were used for functional annotation of DEGs. Protein-protein interaction analyses were performed with STRING. Expression levels of randomly selected DEGs were quantified by real time quantitative polymerase chain reaction (RT-PCR) for validation. Flow cytometry was done to determine frequency of regulatory T cells (Tregs) in PBMC. A total of 361 DEGs (143 upregulated and 218 downregulated) were identified after GeneSpring analysis. DEGs were involved in 28 biological processes, 12 cellular components and 26 molecular functions. Pathway analyses demonstrated that upregulated genes mainly enriched in p53 (CASP3, TSC2, ATR, MDM4, CCNG1) and PI3K/Akt (IL2RA, IL4R, TSC2, VEGFA, PKN2, PIK3CA, ITGA4, BCL2L11) signaling pathways. TP53 and PIK3CA were identified as most significant hub proteins. Expression profiles obtained by RT-PCR were consistent with microarray findings. PD patients showed increased proportions of CD49d+ Tregs, which correlated with disability scores. Survival pathway genes were upregulated putatively to compensate neuronal degeneration. Bioinformatics analysis showed an association between survival and inflammation genes. Increased CD49d+ Treg ratios might signify the effort of the immune system to suppress ongoing neuroinflammation.

CSF levels of HoxB3 and YKL-40 may predict conversion from clinically isolated syndrome to relapsing remitting multiple sclerosis.

INTRODUCTION: Multiple sclerosis (MS) often initiates with an acute episode of neurological disturbance, known as clinically isolated syndrome (CIS). There is an unmet need for biomarkers that differentiate patients who will convert to MS and who will remain as CIS after the first attack. METHODS: First attack serum and cerebrospinal fluid (CSF) samples of 33 CIS patients were collected and these patients were divided as those who converted to MS (CIS-MS, n=17) and those who continued as CIS (CIS-CIS, n=16) in a 3-year follow-up period. Levels of homeobox protein Hox-B3 (HoxB3) and YKL-40 were measured by ELISA in samples of CIS-CIS, CIS-MS, relapsing remitting MS (RRMS) patients (n=15) and healthy controls (n=20). RESULTS: CIS-CIS patients showed significantly reduced CSF levels of YKL-40 and increased serum/CSF levels of HoxB3 compared with CIS-MS and RRMS patients. CIS-MS and RRMS patients had comparable YKL-40 and HoxB3 level profiles. Receiver operating characteristic (ROC) curve analysis showed the highest sensitivity for CSF HoxB3 measurements in prediction of CIS-MS conversion. Kaplan-Meier analysis demonstrated that CIS patients with lower CSF HoxB3 (<3.678 ng/ml) and higher CSF YKL-40 (>654.9 ng/ml) displayed a significantly shorter time to clinically definite MS. CONCLUSION: CSF levels of HoxB3 and YKL-40 appear to predict CIS to MS conversion, especially when applied in combination. HoxB3, which is a transcription factor involved in immune cell activity, stands out as a potential candidate molecule with biomarker capacity for MS.

Impact of Autoimmune Demyelinating Brain Disease Sera on Pericyte Survival.

INTRODUCTION: Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) characterized by demyelination and brain pericyte dysfunction might be involved in MS pathogenesis Our aim was to evaluate whether the factors in serum affect pericyte survival. METHOD: C57BL/6 female mice were immunized with myelin oligodendrocyte glycoprotein (MOG) to induce experimental autoimmune encephalomyelitis (EAE). To confirm the animal model, the sera level of anti-MOG antibody in mice and platelet-derived growth factor-BB (PDGF-BB) in patients was measured by ELISA. Human brain vascular pericytes (HBVP) cell lines were incubated with sera of EAE mice and primer progressive MS (PPMS), seconder progressive MS (SPMS) and relapsing-remitting MS (RRMS) patients. The viability of HBVP is measured with Annexin V-FITC/propidium iodide staining with flow cytometry. RESULTS: Annexin V-FITC/propidium iodide staining with flow cytometry showed increased ratios of early apoptosis and decreased survival following incubation with sera of EAE and progressive MS. Levels of platelet-derived growth factor-BB were identical in serum and cerebrospinal fluids of patients with different forms of MS. CONCLUSION: Our results suggest that serum factors might contribute to progressive MS pathogenesis via pericyte dysfunction.

Functional connectivity analysis of patients with temporal lobe epilepsy displaying different ictal propagation patterns.

The pathophysiology of switch-of lateralization and bilateral temporal asynchrony, which are scalp EEG ictal propagation patterns (iPP) in temporal lobe epilepsy (TLE), is poorly understood. We aimed to analyse functional connectivity (FC) of the temporal lobe and related areas in patients with TLE with iPP (iPP-TLE) and without iPP (non-iPP TLE). Twelve patients with iPP-TLE, 13 patients with non-iPP TLE, and 13 healthy controls (HC) underwent resting-state functional MRI (fMRI). Seed-based FC was analysed between the homologous insulae, hippocampi, amygdalae, parahippocampal, superior temporal, and middle temporal gyri. FC was reduced between homologous temporal lobe areas in patients with TLE compared with HCs. Patients with non-iPP TLE displayed decreased FC between the homologous parahippocampal and superior temporal gyri, and patients with iPP-TLE had lower FC between the homologous insulae, parahippocampal and superior temporal gyri compared with HC. Furthermore, patients with iPP-TLE tended to have lower FC between the bilateral insulae when compared with patients with non-iPP TLE. Reduced FC of interhemispheric connections between temporal lobes and related areas might be an adaptive change to protect contralateral areas in seizure propagation. The insula showed decreased FC between two hemispheres in patients with iPP-TLE, assuming a role in ictal scalp propagation pattern changes in TLE.

A Case of Seronegative Limbic Encephalitis with Multiple Sclerosis: A Possible Overlapping Syndrome.

BACKGROUND Autoimmune encephalitis might coexist in patients with autoimmune demyelinating disorders. CASE REPORT We report on a case of a 45-year-old female multiple sclerosis (MS) patient presenting with acute onset short-term memory loss, altered mental status, inflammatory cerebrospinal fluid (CSF) findings and an MRI lesion on the left temporal lobe. An extensive panel for neuronal autoantibodies proved negative. Neuropsychological symptoms gave a prompt response to immunotherapy but nevertheless control MRI showed left hippocampal atrophy. CONCLUSIONS Several recent reports of concurrent emergence of autoimmune encephalitis and MS suggest a common mechanism for these disorders. Since autoimmune encephalitis and MS share certain common CSF and neuroimaging findings, an increased understanding of overlapping autoimmune brain disorders is required to avoid misdiagnosis especially in antibody negative autoimmune encephalitis cases.

Investigation of neuronal auto-antibodies in systemic lupus erythematosus patients with epilepsy.

PURPOSE: Epilepsy is an important feature for neuropsychiatric involvement in systemic lupus erythematosus (SLE) with unknown mechanism. Our aim was to investigate the presence of neuronal auto-antibodies (NAbs) in neuropsychiatric SLE (NPSLE). METHODS: Eighteen SLE patients (17 females, 1 male) experiencing recurrent seizures were enrolled to this study. Their clinical characteristics, EEG and MRI findings and follow-up information were evaluated from their files. Antibodies against voltage-gated potassium channel (VGKC)-complex antigens, contactin-associated protein-like 2 (CASPR-2), leucine-rich, glioma inactivated 1 (LGI1), glutamic acid decarboxylase (GAD), N-methyl-d-aspartate receptor (NMDA-R), alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid receptor (AMPA-R) and type B gamma aminobutyric acid receptors (GABAB-R) were screened in the sera of these patients. Moreover, indirect immunohistochemistry and immunocytochemistry tests were performed to reveal neuropil antibodies. RESULTS: Six out of 18 patients (33.3%) had various forms of NAbs. Among them, one patient had antibodies against GAD, one patient with hippocampal sclerosis on MRI was CASPR-2 antibody positive, whereas the remaining four patients showed hippocampal neuropil staining. We could not find a significant difference between seropositive and seronegative groups, regarding the clinical characteristics, EEG and MRI findings. CONCLUSION: This study is the first to show hippocampal neuronal staining (4/18) reflecting antibodies against unknown neuronal cell surface antigens in SLE patients with epilepsy, besides the rare occurrence of GAD and CASPR2 antibodies. Further prospective studies are needed to search for new NAbs and uncover their pathogenic role in SLE associated with epilepsy.