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Encephalitis with radial perivascular emphasis | Neurology Neuroimmunology & Neuroinflammation

Encephalitis with radial perivascular emphasis | Neurology Neuroimmunology & Neuroinflammation | AntiNMDA | Scoop.it
Abstract Objective Autoimmune steroid-responsive meningoencephalomyelitis with linear perivascular gadolinium enhancement in brain MRI is regarded as glial fibrillary acidic protein (GFAP) astrocytopathy characterized by anti-GFAP antibodies (ABs). We questioned whether anti-GFAP ABs are necessarily associated with this syndrome. Methods Two patients with a strikingly similar disease course suggestive of autoimmune GFAP astrocytopathy are reported. Clinical examination, MRI, laboratory, and CSF analysis were performed. Neuropathologic examination of brain tissue was obtained from one patient. Serum and CSF were additionally tested using mouse brain slices, microglia-astrocyte cocultures, and a GFAP-specific cell-based assay. Results Both patients presented with subacute influenza-like symptoms and developed severe neurocognitive and neurologic deficits and impaired consciousness. MRIs of both patients revealed radial perivascular gadolinium enhancement extending from the lateral ventricles to the white matter suggestive of autoimmune GFAP astrocytopathy. Both patients responded well to high doses of methylprednisolone. Only one patient had anti-GFAP ABs with a typical staining pattern of astrocytes, whereas serum and CSF of the other patient were negative and showed neither reactivity to brain tissue nor to vital or permeabilized astrocytes. Neuropathologic examination of the anti-GFAP AB-negative patient revealed infiltration of macrophages and T cells around blood vessels and activation of microglia without obvious features of clasmatodendrosis. Conclusions The GFAP-AB negative patient had both a striking (para)clinical similarity and an immediate response to immunotherapy. This supports the hypothesis that the clinical spectrum of steroid-responsive meningoencephalomyelitis suggestive of autoimmune GFAP astrocytopathy may be broader and may comprise also seronegative cases. Glossary AB=antibody; GFAP=glial fibrillary acidic protein; IgG=Immunglobulin G First described in 2016, autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy has been characterized as a rare CNS disorder, typically manifesting as a steroid-responsive encephalitis, meningitis, myelitis, or meningoencephalomyelitis. Neurologic symptoms such as (sub)acute encephalopathy, blurred vision, postural tremor, and seizures often occur following an initial prodromal phase with influenza-like symptoms.1,2 A characteristic feature in brain MRIs is a linear perivascular gadolinium enhancement in the white matter extending radially outward from the ventricles. In addition, extensive lesions of the spinal gray matter may be detected.1 No definite diagnostic criteria have been established yet.3 For diagnosis of autoimmune GFAP astrocytopathy, detection of GFAP antibodies (ABs) in the patient's CSF or serum is required.1 CSF cell count and CSF protein level are usually abnormal. Disease onset has been reported after influenza-like symptoms, a preceding herpes simplex encephalitis, and varicella zoster encephalitis, respectively.1,4 Other ABs, e.g., NMDA receptor IgG and aquaporin-4 IgG may also be detected in autoimmune GFAP astrocytopathy. Furthermore, the disease can be related to an underlying malignancy, with ovarian teratoma being the most common.1 The majority of patients improve after treatment with immunotherapy, especially corticosteroids.2 Yet, the pathophysiology of autoimmune GFAP astrocytopathy is unknown. Here, we compare clinical, radiologic, and serologic findings of two patients with a very similar disease course suggestive of GFAP astrocytopathy. Despite intriguing similarity, only one patient harbored anti-GFAP ABs in serum and CSF. We here discuss that the characteristic clinical syndrome of autoimmune meningoencephalomyelitis with linear perivascular gadolinium enhancement may not necessarily be associated with anti-GFAP ABs. Case report 1 During winter season, a 53-year-old Caucasian man was admitted to hospital due to influenza A infection. In the following weeks, the patient developed cognitive impairment, ataxia, tremor, and a left gaze–evoked nystagmus (for details, see table 1). Cranial MRI revealed areas with diffuse periventricular T2 hyperintensities and linear perivascular gadolinium enhancement in the supratentorial white matter extending radially outward from the ventricles (figure, A). CSF diagnostics revealed 86 cells/μL and 1,075 mg/L protein. High titers of anti-GFAP IgG ABs (titer 1:320) were found in CSF and serum. A typical staining pattern restricted to astrocytes could be detected after incubation of mouse brain slices and astrocyte and microglia cocultures with the patient's CSF. A confirmatory cell-based assay with the GFAPα isoform (Euroimmun, Lübeck, Germany) was positive when incubated with the patient's CSF (figure, B). After other differential diagnoses were ruled out (table 2), autoimmune GFAP astrocytopathy was diagnosed. The patient was treated with methylprednisolone 1000 mg/d for 5 consecutive days. A rapid clinical improvement and a reduction of anti-GFAP IgG AB titers (CSF 1:100, serum 1:100) could be observed. MRI follow-up revealed regressive gadolinium enhancement and decreased periventricular T2 hyperintensities. In addition, EEG follow-up showed improvement with basal alpha activity. When the daily oral prednisolone dose was reduced to less than 20 mg during the following months, the patient's condition deteriorated again as he developed tremor. We therefore initiated 6 cycles of immunoadsorption and subsequently started rituximab treatment. This led to a clinical improvement with almost complete remission of clinical symptoms within 2 weeks. View inline View popup Table 1 Clinical characteristics of case reports 1 and 2 Figure Patients' MRIs, immunofluorescence, and histologic findings Patient 1: (A.a) T2-weighted images demonstrate diffuse periventricular hyperintense lesions (thick arrows, A.a). Axial (A.b) and sagittal (A.c) T1-weighted images with gadolinium show linear perivascular enhancement extending radially through the periventricular white matter (thin arrows). (B) Characteristic staining pattern of GFAP-positive astrocytes in mouse brain slices incubated with CSF of patient 1 (B.a: hippocampus, coronal; magnification ×100; (B.b): Cerebellum, sagittal; magnification ×200). Incubation of astrocyte-microglial cocultures with CSF of patient 1 showed characteristic staining of astrocytes in fixed cells after permeabilization (B.c; magnification ×400), but not in vital cells (B.d; magnification ×200). Incubation of a cell-based assay transfected with the GFAPα isoform with the patient's CSF revealed a positive staining pattern (B.e; magnification ×200). Scale bars: 50 μm each. Patient 2: (C) brain MRI shows similar features as shown in A with periventricular T2 lesions (thick arrows, C.a) and linear perivascular gadolinium enhancement (thin arrows, C.b, C.c). (D) Immunofluorescence stains with CSF of patient 2 revealed no specific staining in brain tissue (D.a: Hippocampus, coronal; magnification ×100; D.b: cerebellum, sagittal; magnification ×200) nor in permeabilized (D.c; magnification ×400) and vital cells (D.d; magnification ×200) in astrocyte-microglial coculture. Incubation of a cell-based assay transfected with the GFAPα isoform with the patient's CSF did not show binding (D.e; magnification ×200). Scale bars: 50 μm each. (E) Histological analysis of patient 2 brain biopsy showed blood vessel–associated infiltration by hematopoietic cells (E.a; hematoxylin and eosin stain; magnification ×200; E.d; CD5-positive T lymphocytes; magnification ×200). Only scattered infiltration by single cytotoxic T cells was observed (E.b; CD8; magnification ×200). The majority of infiltrating cells were identified as macrophages (E.c; CD68; magnification ×200). Brain tissue showed microglial activation (E.e; CD68; magnification ×200) and astrogliosis (E.f; GFAP; magnification ×200), but no obvious signs of clasmatodendrosis. Scale bars: 50 μm each. GFAP = glial fibrillary acidic protein. View inline View popup Table 2 Diagnostics of case reports 1 and 2 before treatment Case report 2 In the same month, a 63-year-old Caucasian man presented with influenza-like symptoms. He later developed cognitive impairment, aggressive behavior, ataxia, and apraxia (for details, see table 1). MRI revealed pronounced T2 hyperintensities and gadolinium enhancement extending radially along the vessels within the supratentorial white matter (figure, C). CSF analysis revealed 53 cells/μL and 2,130 mg/L protein. Repetitive testing for antineuronal, anti-myelin oligodendrocyte glycoprotein, and anti-GFAP ABs was negative including incubation of both the patient's serum and CSF in mouse and monkey brain slices, vital respectively fixed glia cocultures after permeabilization, and a GFAP cell-based assay (figure, D). As most differential diagnoses were ruled out (table 2), the patient underwent frontal brain biopsy. Biopsy featured parenchymal blood vessel associated infiltration of macrophages and T cells. Brain tissue itself showed activation of microglia, infiltration of macrophages, and astrogliosis (figure, E). Although not specific, histopathologic findings are compatible with the few available histology reports of proven cases of autoimmune GFAP astrocytopathy in the literature.5 We did not observe direct signs of clasmatodendrosis or loss of aquaporin-4 (not shown), which is typically seen in anti–aquaporin-4 AB-positive neuromyelitis optica spectrum disorder. Following treatment with IV immunoglobulins, the patient's condition deteriorated as he developed brainstem symptoms including dysarthria, dysphagia, and impaired consciousness. Artificial ventilation was required. Following methylprednisolone pulse therapy of 1000 mg/d for 5 consecutive days, a rapid clinical improvement was observed, and the patient could be extubated and was able to eat and walk again. Brain MRI confirmed a significant regression of T2 lesions and decreased radial perivascular gadolinium enhancement. Thus, oral prednisolone treatment was continued and tapered over the next months. EEG follow-up showed a significant improvement with basic alpha but still intermittent bifrontal delta activity. CSF measurement 3 months after first hospital admission revealed lower but still increased cell count (33 cells/μL) and protein levels (1,100 mg/L protein). Thereafter, 5 cycles of immunoadsorption were initiated with subsequent clinical improvement. However, after tapering prednisolone to less than 10 mg daily symptoms reoccurred, MRI demonstrated radial perivascular gadolinium enhancement, and CSF showed a persistent pleocytosis of 31 cells/μL. Additional treatment with azathioprine was initiated, and prednisolone was increased to 80 mg again and tapered over the following months. Discussion Detection of anti-GFAP ABs and typical MRI findings are regarded as essential features in the diagnosis of autoimmune GFAP astrocytopathy. We here compare two patients with a similar disease course suggestive of autoimmune GFAP astrocytopathy. Yet, only in one patient, anti-GFAP ABs were detected. Recent reports questioned the relevance of anti-GFAP ABs in this clinical syndrome.3,6 In line with these reports, we here support the hypothesis that autoimmune meningoencephalomyelitis with characteristic MRI findings and steroid responsiveness may present with diverse immunologic findings, and the presence of anti-GFAP ABs is not obligatory. So far, it is not clear whether the presence of anti-GFAP-ABs in some patients with this disorder is just an immunologic accompaniment or whether these patients with anti-GFAP-ABs represent a particular subgroup with a specific pathophysiology targeting the astrocyte. Because anti-GFAP ABs bind to astrocytic cytosolic intermediate filaments and ABs are not internalized, a direct pathophysiologic relevance of these ABs is unlikely. As known from autoimmune encephalitis and neuromyelitis optica spectrum disorders, pathophysiologically relevant ABs usually target membrane surface proteins.7 In contrast, in paraneoplastic disorders, specific onconeuronal ABs to intracellular antigens are not pathogenic but excellent biomarkers.7 In autoimmune GFAP astrocytopathy, a role of autoreactive T cells triggering a GFAP-specific autoimmune response has been suggested.3 In a rat model, CD3+ T cells have been shown in close proximity to GFAP-positive astrocytes, thereby inducing an immune response with production of IgG ABs to GFAP.8 This might be a first direct link of how the humoral response is initiated. Of note, in our patients and also in others, an observational link exists between viral infections, e.g., influenza A, herpes simplex, and varicella zoster and subsequent GFAP autoimmunity.1 The association of viral CNS infections and other forms of autoimmune encephalitis is well established. Here, antigen presentation due to neuronal damage caused by viral inflammation or virus-induced costimulation of immune cells is favored to be a pathophysiologic mechanism involved in promoting encephalitis.9 Although influenza A infection does not necessarily lead to neuronal damage in the CNS, it may be a predisposing factor to develop GFAP autoimmunity. The specificity of anti-GFAP ABs for meningoencephalomyelitis needs to be clarified in further studies, as serum anti-GFAP ABs can also be found in other diseases, e.g., traumatic brain injury, vascular dementia, and astrocytoma, or even in healthy controls.10 Study funding This study was funded by the Schilling Foundation (to C. Geis); Center for Sepsis Control and Care (CSCC; to C. Geis and J. Wickel); and Interdisciplinary Center for Clinical Research Jena University Hospital (IZKF; to H-Y. Chung and J. Wickel). Disclosure In the preparation of this manuscript, the funding sources played no role. J. Wickel, H.-Y. Chung, K. Kirchhof, and D. Boeckler report no disclosures. S. Merkelbach received travel funding, speaker, and/or advisory board honoraria from Bayer, Biogen, Daiichi Sankyo, Genzyme, and Merck Serono. P. Kuzman and W. C. Mueller report no disclosures. C. Geis received advisory board honoraria and speaker honoraria from Roche and Alexion and received research support from the Schilling Foundation, the German Research Council, and the German Ministry of Education. A. Günther received travel funding, speaker, and/or advisory board honoraria from Merz, Ipsen, Boehringer Ingelheim, Pfizer, Daiichi Sankyo, and Bayer. Go to Neurology.org/NN for full disclosures. Acknowledgment The authors thank the patients for their participation in this study and Claudia Sommer for excellent technical assistance. Furthermore, they thank Euroimmun (Lübeck, Germany) for their support in antibody diagnostics and Prof. Dr. Christine Stadelmann-Nessler and Dr. Jonas Franz (Institute of Neuropathology, University Medical Center Göttingen, Germany) for providing histological staining of aquaporin 1 and 4. Appendix Authors Footnotes Go to Neurology.org/NN for full disclosures. Funding information is provided at the end of the article. ↵* These authors contributed equally to the manuscript. ↵† Shared seniority. The Article Processing Charge was funded by the authors. Received September 4, 2019. Accepted in final form November 26, 2019. Copyright © 2020 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND), which permits downloading and sharing the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. References 1.↵Flanagan EP, Hinson SR, Lennon VA, et al. Glial fibrillary acidic protein immunoglobulin G as biomarker of autoimmune astrocytopathy: analysis of 102 patients. Ann Neurol 2017;81:298–309.OpenUrl 2.↵Iorio R, Damato V, Evoli A, et al. Clinical and immunological characteristics of the spectrum of GFAP autoimmunity: a case series of 22 patients. J Neurol Neurosurg Psychiatry 2018;89:138–146. 3.↵Shan F, Long Y, Qiu W. Autoimmune glial fibrillary acidic protein astrocytopathy: a review of the literature. Front Immunol 2018;9:2802.OpenUrl 4.↵Fang B, McKeon A, Hinson SR, et al. Autoimmune glial fibrillary acidic protein astrocytopathy: a novel meningoencephalomyelitis. JAMA Neurol 2016;73:1297–1307.OpenUrl 5.↵Shu Y, Long Y, Chang Y, et al. Brain immunohistopathology in a patient with autoimmune glial fibrillary acidic protein astrocytopathy. Neuroimmunomodulation 2018;25:1–6.OpenUrl 6.↵Xie L, Liu T, Yao H, et al. Autoimmune inflammatory meningoencephalitis in a patient negative for glial fibrillary acidic protein-specific immunoglobulin G. Mult Scler Relat Disord 2019;28:167–171.OpenUrl 7.↵Dalmau J, Geis C, Graus F. Autoantibodies to synaptic receptors and neuronal cell surface proteins in autoimmune diseases of the central nervous system. Physiol Rev 2017;97:839–887.OpenUrlCrossRefPubMed 8.↵Park ES, Uchida K, Nakayama H. Establishment of a rat model for canine necrotizing meningoencephalitis (NME). Vet Pathol 2014;51:1151–1164.OpenUrlCrossRefPubMed 9.↵Armangue T, Leypoldt F, Málaga I, et al. Herpes simplex virus encephalitis is a trigger of brain autoimmunity. Ann Neurol 2014;75:317–323.OpenUrlCrossRefPubMed 10.↵Wang KK, Yang Z, Yue JK, et al. Plasma anti-glial fibrillary acidic protein autoantibody levels during the acute and chronic phases of traumatic brain injury: a transforming research and clinical knowledge in traumatic brain injury pilot study. J Neurotrauma 2016;33:1270–1277.OpenUrlCrossRef
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Neural Antibody Testing in Patients with Suspected Autoimmune Encephalitis | Clinical Chemistry | Oxford Academic

Neural Antibody Testing in Patients with Suspected Autoimmune Encephalitis | Clinical Chemistry | Oxford Academic | AntiNMDA | Scoop.it
AbstractBackground. Autoimmunity is an increasingly recognized cause of encephalitis with a similar prevalence to that of infectious etiologies. Over the past d
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Pathophysiology of paraneoplastic and autoimmune encephalitis: genes, infections, and checkpoint inhibitors - Alberto Vogrig, Sergio Muñiz-Castrillo, Virginie Desestret, Bastien Joubert, Jérôme Hon...

Pathophysiology of paraneoplastic and autoimmune encephalitis: genes, infections, and checkpoint inhibitors - Alberto Vogrig, Sergio Muñiz-Castrillo, Virginie Desestret, Bastien Joubert, Jérôme Hon... | AntiNMDA | Scoop.it
Paraneoplastic neurological syndromes (PNSs) are rare complications of systemic cancers that can affect all parts of the central and/or peripheral nervous system. A body of experimental and clinica...
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Relationship between serum NMDA receptor antibodies and response to antipsychotic treatment in first episode psychosis

Relationship between serum NMDA receptor antibodies and response to antipsychotic treatment in first episode psychosis | AntiNMDA | Scoop.it
When psychosis develops in NMDAR antibody encephalitis it usually has an acute or
subacute onset, and antipsychotic treatment may be ineffective and associated with
adverse effects. Serum NMDAR antibodies have been reported in a minority of patients with first episode psychosis (FEP), but their...
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https://www.researchgate.net/publication/343817904_Anti-N-methyl-D-Aspartate_NMDA_Receptor_Encephalitis_A_Case_Report

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Defying the odds, U of T's Carisse Samuel to graduate after spending five months in a coma

Defying the odds, U of T's Carisse Samuel to graduate after spending five months in a coma | AntiNMDA | Scoop.it
When Carisse Samuel joins her fellow graduates at the University of Toronto’s virtual convocation this Saturday, the celebration will be both an academic and personal victory.
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Clinical features which predict neuronal surface autoantibodies in new-onset focal epilepsy: implications for immunotherapies | Journal of Neurology, Neurosurgery & Psychiatry

Introduction Neuronal surface-directed antibodies (NSAbs) are considered pathogenic in patients with autoimmune encephalitis (AE). AE commonly presents with prominent seizures and neuropsychiatric features and shows a preferential response to immunotherapies versus anti-seizure medications (ASMs).1–4 This has prompted the introduction of ‘epilepsy of immune aetiology’ within the International League Against Epilepsy (ILAE) 2017 classification.5 The same NSAbs, as well as high levels of antibodies to intraneuronal glutamic acid decarboxylase-65 (GAD65), are also described in the serum of people with more isolated forms of epilepsy, without core features of encephalitis.6–8 In this context, their clinical, aetiological and therapeutic relevance is unclear, but of major potential importance to all neurologists who manage new-onset epilepsy. In our large, prospective, real-world study of new-onset focal epilepsy, we predicted that formes frustes of AE would help identify clinical features suggesting the presence of NSAbs and asked whether detection of these NSAbs should alter patient management. Materials and methods Between 9 December 2011 and 4 November 2015, consecutive adult patients (≥18 years) with a diagnosis of new-onset focal epilepsy and their first seizure within the previous 12 months were prospectively recruited from the routine practice of two epileptologists at the Oxford University Hospitals NHS Foundation Trust. Written informed consent and sera were obtained (Ethical approvals: Oxfordshire RECA 07/Q160X/28 and REC16/YH/0013). Clinical data gathered at onset (online supplemental table 1) included detailed phenotype and investigation results, Quality of Life in Epilepsy-31, Hospital Anxiety and Depression Score, Addenbrooke’s Cognitive Examination (ACE) and modified Rankin Score (mRS); as well as information to inform the Antibody Prevalence in Epilepsy and Encephalopathy (APE2) score (online supplemental table 2)9 10 and diagnostic criteria for possible or definite AE.11 Subsequently, 1-year and 3-year mRS were ascertained from patients with NSAbs. Supplemental material For NSAbs, sera were tested against autoantigen-expressing live HEK293 cells (live cell-based assay; online supplemental table 3), and for reactivity with the surface of live cultured hippocampal neurons, using sensitive protocols.12 13 Autoantibodies to GAD65 were determined using a commercial radioimmunoprecipitation assay. Statistical analysis was conducted in R (V.3.6.1). Dimensionality reduction was performed using Multiple Factor Analysis in ‘FactoMineR’ with up to 10% missing data imputed using missForest. Stepwise Bayesian general linear modelling analysis was undertaken using ‘arm’. Wilson 95% CIs with continuity correction were calculated using ‘DescTools’. Results NSAb findings Of 241 recruited patients, 22 were excluded (online supplemental table 4). Of the remaining 219, median age was 49 years (range 16–91) and 109 (49.8%) were female. In 23/219 (10.5%) patients, serum NSAbs were detected across candidate and novel autoantigens (table 1) including roughly equal frequencies against leucine-rich glioma inactivated-1 (LGI1), contactin-associated protein-like 2 (CASPR2), plus the N-methyl-d-aspartate receptor (NMDAR) and γ-aminobutyric acid A/B receptors (GABAAR and GABABR). An additional five patients had antibodies to the surface of live neurons, without an established autoantigen. Autoantibodies to contactin-2, the glycine receptor and the α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) were each found in one patient. No dipeptidyl-peptidase-like protein 6 (DPPX) or high-titre GAD65 antibodies were detected. Overall, from the 23 people with NSAbs, 9 had a clinical diagnosis of AE (7/9 fulfilling published criteria).11 By contrast, none of the 196 without NSAbs had a clinical diagnosis of AE (p<0.0001; Fisher’s exact test). VIEW INLINE VIEW POPUP Table 1 Clinical and laboratory features of patients with epilepsy and positive neuronal surface autoantibodies Factors associated with the presence of NSAbs and AE Dimensionality reduction with multiple factor analysis showed that patients were highly heterogeneous and the modest clustering of those with NSAbs was largely driven by a clinical diagnosis of AE (figure 1A,B). Univariate analysis identified 11 clinical parameters that differed significantly between patients with and without NSAbs: age (p=0.04), ictal piloerection (p=0.02), lesional MRI (p=0.04), self-reported mood disturbance (p=0.007), ACE attention domain (p=0.01), ACE total score (p=0.04), QOLIE-31 score (p=0.02), self-reported neuropsychiatric features (p=0.03), epilepsy risk factors (p=0.05), inflammatory cerebrospinal fluid (CSF; p=0.004) and limbic system lesions on MRI (p=0.0002). A multivariate stepwise regression model allocated weighted scores to six of these: age ≥54 years=+1, self-reported mood disturbance=+1, limbic system lesions on MRI=+2, ictal piloerection=+2.5, ACE attention score ≥16=−1.5 and epilepsy risk factors=−1.5 (figure 1C). The probability of NSAb positivity increased with higher scores (Spearman’s ρ=0.99, p<0.0001; figure 1C) and receiver operating characteristic (ROC) analysis confirmed these features strongly predicted NSAb status (area under the curve (AUC)=0.83; total score ≥0; sensitivity=66.7%, specificity=84.9%; figure 1D). By contrast, the APE2 score performed less well in predicting NSAb status (sensitivity 43.5%, specificity 79.1%, AUC=0.68) and more accurately predicted criteria-defined AE, particularly if associated with NSAbs (sensitivity 85.7%, specificity 78.8%, AUC=0.94; figure 1E). Figure 1 Clinical phenotypes associated with NSAb status in new-onset focal epilepsy. The first two dimensions are shown, highlighting: (A) NSAb-positive (red) or NSAb-negative (grey) status and (B) NSAb-positive (pale red) or NSAb-negative (grey) without encephalitis (dots), or NSAb-positive (dark red) with clinically diagnosed autoimmune encephalitis (triangles). (C) The proportion of patients by total model score. Error bars show 95% CIs. The inset shows the weighting and SE of each factor within the regression model. (D) Receiver operator characteristic (ROC) curve of the total model score for predicting NSAb status across all patients. (E) ROC curve of the APE2 score for predicting NSAb status across all patients (black), patients not meeting the criteria for autoimmune encephalitis (blue), patients meeting the criteria for autoimmune encephalitis (red) and predicting NSAb-positive criteria-confirmed autoimmune encephalitis across all patients. (F) Scatter plot of modified Rankin score in NSAb-positive patients by immunotherapy status over time (Mann-Whitney U test p values<0.05). AE, autoimmune encephalitis; APE2, Antibody Prevalence in Epilepsy and Encephalopathy; epilepsy RF, epilepsy risk factors; MRI limbic Δ, changes within the limbic system on MRI. Comparisons of those with and without AE From 23 patients with NSAbs (table 1), a comparison of those with (n=9) and without (n=14) a clinical diagnosis of AE revealed several differences in the AE cohort: more ASMs (median of 3 vs 1; p=0.0073), more frequent immunotherapies (7/9 vs 0/14, p=0.0001), higher APE2 scores (median of 6 vs 2; p<0.0001), more frequent MRI limbic inflammation (6/9 vs 0/14; p=0.0008) and a trend towards greater positivity of serum IgGs targeting the surface of live neurons (7/9 vs 5/14, p=0.09). Compared with the seven patients administered immunotherapy, those with NSAbs who were not administered immunotherapy showed lower disability after 1 and 3 years (both p<0.05), and 11/16 (68.8%) were asymptomatic at 3-year follow-up (mRS=0 ; figure 1F). Hence, despite no immunotherapy, patients with NSAbs, but without AE, generally showed good outcomes. Discussion In this prospective study of 219 consecutive adults with new-onset focal epilepsy, NSAb status was best predicted by a combination of clinical parameters which closely resemble features observed in AE. Almost half of our patients with NSAbs were diagnosed with AE, and ~30% fulfilled stringent criteria for AE.11 Of those with NSAbs and more isolated forms of epilepsy, without individual features of AE, almost all were treated with ASMs alone and typically remained asymptomatic at long-term follow-up. Overall, these findings suggest that detection of NSAbs in patients with new-onset seizures, but without features of AE, should not alter current clinical management. Our observations should help guide the frequent clinical dilemma of which patients with new-onset seizures to test for autoantibodies and subsequently treat with immunotherapy. Taken together, our data suggest the clinical phenotype is paramount in guiding the relevance of autoantibody results, and provide data to address an outstanding question from a recent ILAE consensus statement.7 This ILAE statement also highlighted controversy over the term ‘autoimmune epilepsy’.7 In routine clinical practice, this nomenclature acts as a valuable signpost and aide memoire when seeing patients with seizures.2 14 However, ‘epilepsy’ carries several social stigmata and is defined by an enduring tendency to seizures. In AE, this lifelong risk is refuted by a recent study,4 despite several forms of AE commonly leading to hippocampal atrophy.2–4 7 10 The alternative concept of acute symptomatic seizures may more accurately capture the nature of seizures in patients with AE. Data-driven modifications to nomenclature will benefit from longer-term follow-up studies. Ictal piloerection, low mood and attention and MRI limbic system changes are recognised features of late-onset AE, particularly in association with LGI1 antibodies.2 4 14 15 The absence of movement disorders or more diffuse cognitive impairment as predictive factors in our model suggests the overall syndrome may reflect a formes frustes of AE. This contrasts with APE2 score parameters,9 which appear to largely reflect more florid features seen in classical AE. Our observational study has several limitations. These include limited CSF autoantibody measurements, which reflected UK practice particularly at the start of the study period. Yet,w ithout this valuable parameter, a diagnosis of NMDAR-antibody encephalitis is still possible.11 Yet, two of our four patients with serum NMDAR antibodies did not have features consistent with encephalitis, likely suggesting detection of clinically unrelated serum antibodies in these cases. In addition, our series in total only identified nine AE cases, although this may be considered substantial given the largely outpatient-based recruitment. This, and the high (~10%) seroprevalence rate, may reflect a referral bias given Oxford’s interest in AE, but is well aligned with other available estimates.6 9 10 Our serological data identified some samples with NSAbs proven by live cell-based assays, but without concomitant cell surface neuronal reactivities. This was especially evident in the cohort without a clinical diagnosis of AE, and perhaps these antibodies reflect low-affinity or low-titre autoantibodies which are not disease relevant. Their specificity, however, remains reassuring given their typical selectivity for just one of eight surface-expressed autoantigens. In the future, our prediction model will benefit from validation in independent, larger studies which may compare the risk of enduring seizures in the NSAb-positive versus NSAb-negative populations, with and without AE, something which we did not survey at follow-up. Hence, we cannot comment on long-term seizure status in the 5/16 patients (31%) who had NSAbs, no diagnosis of AE and 3-year mRS >0. In these patients, it remains possible that immunotherapy would have led to a greater benefit. However, in our view, this finding is more likely to be consistent with the predicted ~30% of all people with epilepsy who are known to become ASM resistant: this provides a testable hypothesis for a future randomised controlled trial. Overall, our observations support the concept that, in patients who present with new-onset focal seizures, clinical features which are consistent with a ‘mild encephalitis’ helps identify those with NSAbs which should alter patient management. This clinico-serological syndrome appeared characteristic and its recognition will improve detection and treatment of these patients. These findings should discourage widespread screening strategies to identify patients with autoantibodies among unselected seizure cohorts. References ↵Irani SR, Michell AW, Lang B, et al. Faciobrachial dystonic seizures precede Lgi1 antibody limbic encephalitis. Ann Neurol 2011;69:892–900.doi:10.1002/ana.22307 ↵Thompson J, Bi M, Murchison AG, et al. The importance of early immunotherapy in patients with faciobrachial dystonic seizures. Brain 2018;141:348–56.doi:10.1093/brain/awx323OpenUrlCrossRef ↵Geis C, Planagumà J, Carreño M, et al. Autoimmune seizures and epilepsy. J Clin Invest 2019;129:926–40.doi:10.1172/JCI125178OpenUrlPubMed ↵de Bruijn MAAM, van Sonderen A, van Coevorden-Hameete MH, et al. Evaluation of seizure treatment in anti-LGI1, anti-NMDAR, and anti-GABABR encephalitis. Neurology 2019;92:e2185–96.doi:10.1212/WNL.0000000000007475pmid:30979857OpenUrlPubMed ↵Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: position paper of the ILAE Commission for Classification and Terminology. Epilepsia 2017;58:512–21.doi:10.1111/epi.13709pmid:http://www.ncbi.nlm.nih.gov/pubmed/28276062OpenUrlPubMed ↵Brenner T, Sills GJ, Hart Y, et al. Prevalence of neurologic autoantibodies in cohorts of patients with new and established epilepsy. Epilepsia 2013;54:1028–35.doi:10.1111/epi.12127pmid:http://www.ncbi.nlm.nih.gov/pubmed/23464826OpenUrlCrossRefPubMed ↵Steriade C, Britton J, Dale RC, et al. Acute symptomatic seizures secondary to autoimmune encephalitis and autoimmune-associated epilepsy: conceptual definitions. Epilepsia 2020;61:1341–51.doi:10.1111/epi.16571pmid:http://www.ncbi.nlm.nih.gov/pubmed/32544279OpenUrlPubMed ↵von Podewils F, Suesse M, Geithner J, et al. Prevalence and outcome of late-onset seizures due to autoimmune etiology: a prospective observational population-based cohort study. Epilepsia 2017;58:1542–50.doi:10.1111/epi.13834pmid:http://www.ncbi.nlm.nih.gov/pubmed/28681401OpenUrlPubMed ↵Dubey D, Alqallaf A, Hays R, et al. Neurological autoantibody prevalence in epilepsy of unknown etiology. JAMA Neurol 2017;74:397–402.doi:10.1001/jamaneurol.2016.5429pmid:http://www.ncbi.nlm.nih.gov/pubmed/28166327OpenUrlPubMed ↵Dubey D, Kothapalli N, McKeon A, et al. Predictors of neural-specific autoantibodies and immunotherapy response in patients with cognitive dysfunction. J Neuroimmunol 2018;323:62–72.doi:10.1016/j.jneuroim.2018.07.009pmid:http://www.ncbi.nlm.nih.gov/pubmed/30196836OpenUrlPubMed ↵Graus F, Titulaer MJ, Balu R, et al. A clinical approach to diagnosis of autoimmune encephalitis. Lancet Neurol 2016;15:391–404.doi:10.1016/S1474-4422(15)00401-9pmid:http://www.ncbi.nlm.nih.gov/pubmed/26906964OpenUrlCrossRefPubMed ↵Makuch M, Wilson R, Al-Diwani A, et al. N-Methyl-D-aspartate receptor antibody production from germinal center reactions: therapeutic implications. Ann Neurol 2018;83:553–61.doi:10.1002/ana.25173pmid:http://www.ncbi.nlm.nih.gov/pubmed/29406578OpenUrlPubMed ↵Ramberger M, Berretta A, Tan JMM, et al. Distinctive binding properties of human monoclonal LGI1 autoantibodies determine pathogenic mechanisms. Brain 2020;143:1731–45.doi:10.1093/brain/awaa104pmid:http://www.ncbi.nlm.nih.gov/pubmed/32437528OpenUrlPubMed ↵Quek AML, Britton JW, McKeon A, et al. Autoimmune epilepsy: clinical characteristics and response to immunotherapy. Arch Neurol 2012;69:582–93.doi:10.1001/archneurol.2011.2985pmid:http://www.ncbi.nlm.nih.gov/pubmed/22451162OpenUrlCrossRefPubMed ↵Rocamora R, Becerra JL, Fossas P, et al. Pilomotor seizures: an autonomic semiology of limbic encephalitis? Seizure 2014;23:670–3.doi:10.1016/j.seizure.2014.04.013pmid:http://www.ncbi.nlm.nih.gov/pubmed/24890932OpenUrlCrossRefPubMed
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Sleep disorders in autoimmune encephalitis

Sleep disorders in autoimmune encephalitis | AntiNMDA | Scoop.it
Sleep disorders in people with autoimmune encephalitis have received little attention,
probably overshadowed by the presence of other neurological and psychiatric symptoms
in this group of conditions.
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Cerebrospinal fluid CD20 positive B-cell expansion in a case of anti-NMDAR encephalitis - ScienceDirect

Cerebrospinal fluid CD20 positive B-cell expansion in a case of anti-NMDAR encephalitis - ScienceDirect | AntiNMDA | Scoop.it
Anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis is a potentially fatal autoimmune encephalitis with a strong B-cell response. We measured the …
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Clinical, cognitive and neuroanatomical associations of serum NMDAR autoantibodies in people at clinical high risk for psychosis

Clinical, cognitive and neuroanatomical associations of serum NMDAR autoantibodies in people at clinical high risk for psychosis | AntiNMDA | Scoop.it
Serum neuronal autoantibodies, such as those to the NMDA receptor (NMDAR), are detectable in a subgroup of patients with psychotic disorders. It is not known if they are present before the onset of psychosis or whether they are associated with particular clinical features or outcomes. In a case–control study, sera from 254 subjects at clinical high risk (CHR) for psychosis and 116 healthy volunteers were tested for antibodies against multiple neuronal antigens implicated in CNS autoimmune disorders, using fixed and live cell-based assays (CBAs). Within the CHR group, the relationship between NMDAR antibodies and symptoms, cognitive function and clinical outcomes over 24 month follow-up was examined. CHR subjects were not more frequently seropositive for neuronal autoantibodies than controls (8.3% vs. 5.2%; OR = 1.50; 95% CI: 0.58–3.90). The NMDAR was the most common target antigen and NMDAR IgGs were more sensitively detected with live versus fixed CBAs (p < 0.001). Preliminary phenotypic analyses revealed that within the CHR sample, the NMDAR antibody seropositive subjects had higher levels of current depression, performed worse on the Rey Auditory Verbal Learning Task (p < 0.05), and had a markedly lower IQ (p < 0.01). NMDAR IgGs were not more frequent in subjects who later became psychotic than those who did not. NMDAR antibody serostatus and titre was associated with poorer levels of functioning at follow-up (p < 0.05) and the presence of a neuronal autoantibody was associated with larger amygdala volumes (p < 0.05). Altogether, these findings demonstrate that NMDAR autoantibodies are detectable in a subgroup of CHR subjects at equal rates to controls. In the CHR group, they are associated with affective psychopathology, impairments in verbal memory, and overall cognitive function: these findings are qualitatively and individually similar to core features of autoimmune encephalitis and/or animal models of NMDAR antibody-mediated CNS disease. Overall the current work supports further evaluation of NMDAR autoantibodies as a possible prognostic biomarker and aetiological factor in a subset of people already meeting CHR criteria.
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Longitudinal measurement of CSF neurofilament light in anti‐NMDAR encephalitis - Macher - - European Journal of Neurology

Longitudinal measurement of CSF neurofilament light in anti‐NMDAR encephalitis - Macher - - European Journal of Neurology | AntiNMDA | Scoop.it
Abstract Background Biomarkers reflecting the course of patients suffering from anti‐NMDAR encephalitis (anti‐NMDARE) are urgently needed. Neurofilament light chains (NfL) have been studied as a po...
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Brain researcher: It’s difficult to separate the physical and mental when it comes to our brains

Brain researcher: It’s difficult to separate the physical and mental when it comes to our brains | AntiNMDA | Scoop.it
Emotions, mental ailments, brain diseases: Everything happens in the brain. Technological advances have given us new perspectives on how the brain works, according to Norwegian brain researchers.
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Specialists and Care Centers for Autoimmune Encephalitis

Specialists and Care Centers for Autoimmune Encephalitis | AntiNMDA | Scoop.it
The Northwestern Medicine Autoimmune Encephalitis and Paraneoplastic Disorders clinic takes a multidiscplinary approach to the diagnosis and care of patients affected by these disorders.
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Neurologic Emergencies at the Extremes of Age

Neurologic Emergencies at the Extremes of Age | AntiNMDA | Scoop.it
The diagnosis and management of neurologic conditions are more complex at the extremes
of age than in the average adult. In the pediatric population, neurologic emergencies
are somewhat rare and some may require emergent consultation.
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(PDF) Anti-N-methyl-D-Aspartate (NMDA) Receptor Encephalitis: A Case Report

(PDF) Anti-N-methyl-D-Aspartate (NMDA) Receptor Encephalitis: A Case Report | AntiNMDA | Scoop.it
PDF | We report case of a 42 years old female who came with a constellation of behavioral symptoms, delirium, body stiffness, and fever for one week....| Find, read and cite all the research you need on ResearchGate...
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RACGP - Old doc, new disease: Anti-NMDA receptor encephalitis

RACGP - Old doc, new disease: Anti-NMDA receptor encephalitis | AntiNMDA | Scoop.it
Dr Casey Parker reflects on an intriguing presentation that made him ask: What else do I not know?
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Cost-Effectiveness of Routine Screening for Autoimmune Encephalitis in Patients With First-Episode Psychosis in the United States |J Clin Psychiatry

Autoimmune encephalitis (AE) is a highly treatable neurologic condition that can cause psychosis. This study estimated the cost-effectiveness of routine screening for AE compared with clinically targeted screening in first-episode psychosis patients.
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Unremitting diarrhoea in a girl diagnosed anti-N-methyl-D-aspartate-receptor encephalitis: A case report | Read by QxMD

Unremitting diarrhoea in a girl diagnosed anti-N-methyl-D-aspartate-receptor encephalitis: A case report | Read by QxMD | AntiNMDA | Scoop.it
Create a free QxMD account to take advantage of the features offered by Read like saving your papers and creating collections. Get Started Unremitting diarrhoea in a girl diagnosed anti-N-methyl-D-aspartate-receptor encephalitis: A case report Norrapat Onpoaree, Montida Veeravigrom, Anapat Sanpavat, Narissara Suratannon, Palittiya Sintusek World Journal of Clinical Cases 2020 October 26, 8 (20): 4866-4875 BACKGROUND: Asymptomatic cytomegalovirus (CMV) infection is common in children; in contrast, in children with a weakened immune system, invasive CMV can occur. This is the first case report of a severe manifestation of CMV esophago-enterocolitis in a girl diagnosed with anti-N-methyl-D-aspartate-receptor (anti-NMDAR) encephalitis who received only a moderate dose of corticosteroid therapy. CASE SUMMARY: A 12-year-old-Thai girl presented with acute behavioural change and headache for 6 d. Electroencephalogram and positivity for NMDAR autoantibodies were compatible with anti-NMDAR encephalitis. Hence, she received pulse methylprednisolone 10 mg/kg per day for 4 d and continued with prednisolone 1.2 mg/kg per day. On day 42 of corticosteroid therapy, she developed unremitting vomiting and diarrhoea. Endoscopy showed multiple ulcers and erythaematous mucosa along the gastrointestinal tract. Tissue CMV viral load and viral-infected cells confirmed CMV esophago-enterocolitis. Therefore, the patient received ganciclovir 5 mg/kg per dose every 12 h for 3 wk and then 5 mg/kg per dose once daily for 3 wk. Unremitting diarrhoea slowly improved from stool output 1-4 L per day to 1-2 L per day after 3 wk of treatment. Pulse methylprednisolone 20 mg/kg for 5 d was initiated and continued with prednisolone 1 mg/kg per day. After this repeated pulse methylprednisolone treatment, surprisingly, diarrhoea subsided. Immunologic work-up was performed to rule out underlying immune deficiency with unremarkable results. CONCLUSION: Unremitting diarrhoea from CMV esophago-enterocolitis subsided with antiviral and methylprednisolone therapy, implying the immune and NMDAR dysregulation in anti-NMDAR encephalitis. Full Text Links We have located links that may give you full text access. Additional links Discussion You are not logged in. Sign Up or Log In to join the discussion. Trending Papers Colchicine in Patients with Chronic Coronary Disease. Stefan M Nidorf, Aernoud T L Fiolet, Arend Mosterd, John W Eikelboom, Astrid Schut, Tjerk S J Opstal, Salem H K The, Xiao-Fang Xu, Mark A Ireland, Timo Lenderink, Donald Latchem, Pieter Hoogslag, Anastazia Jerzewski, Peter Nierop, Alan Whelan, Randall Hendriks, Henk Swart, Jeroen Schaap, Aaf F M Kuijper, Maarten W J van Hessen, Pradyot Saklani, Isabel Tan, Angus G Thompson, Allison Morton, Chris Judkins, Willem A Bax, Maurits Dirksen, Marco M W Alings, Graeme J Hankey, Charley A Budgeon, Jan G P Tijssen, Jan H Cornel, Peter L Thompson New England Journal of Medicine 2020 August 31 Extracorporeal life support for adults with acute respiratory distress syndrome. Alain Combes, Matthieu Schmidt, Carol L Hodgson, Eddy Fan, Niall D Ferguson, John F Fraser, Samir Jaber, Antonio Pesenti, Marco Ranieri, Kathryn Rowan, Kiran Shekar, Arthur S Slutsky, Daniel Brodie Intensive Care Medicine 2020 November 2 Clinical strategies for implementing lung and diaphragm-protective ventilation: avoiding insufficient and excessive effort. Ewan C Goligher, Annemijn H Jonkman, Jose Dianti, Katerina Vaporidi, Jeremy R Beitler, Bhakti K Patel, Takeshi Yoshida, Samir Jaber, Martin Dres, Tommaso Mauri, Giacomo Bellani, Alexandre Demoule, Laurent Brochard, Leo Heunks Intensive Care Medicine 2020 November 2 Emergency Department Management of COVID-19: An Evidence-Based Approach. Nicholas M McManus, Ryan Offman, Jason D Oetman Western Journal of Emergency Medicine 2020 September 25 Glucocorticoids: surprising new findings on their mechanisms of actions. Frank Buttgereit Annals of the Rheumatic Diseases 2020 November 8 Prone position in ARDS patients: why, when, how and for whom. Claude Guérin, Richard K Albert, Jeremy Beitler, Luciano Gattinoni, Samir Jaber, John J Marini, Laveena Munshi, Laurent Papazian, Antonio Pesenti, Antoine Vieillard-Baron, Jordi Mancebo Intensive Care Medicine 2020 November 10 Severe organising pneumonia following COVID-19. István Vadász, Faeq Husain-Syed, Peter Dorfmüller, Fritz C Roller, Khodr Tello, Matthias Hecker, Rory E Morty, Stefan Gattenlöhner, Hans-Dieter Walmrath, Friedrich Grimminger, Susanne Herold, Werner Seeger Thorax 2020 November 11 Analgesia and sedation in patients with ARDS. Gerald Chanques, Jean-Michel Constantin, John W Devlin, E Wesley Ely, Gilles L Fraser, Céline Gélinas, Timothy D Girard, Claude Guérin, Matthieu Jabaudon, Samir Jaber, Sangeeta Mehta, Thomas Langer, Michael J Murray, Pratik Pandharipande, Bhakti Patel, Jean-François Payen, Kathleen Puntillo, Bram Rochwerg, Yahya Shehabi, Thomas Strøm, Hanne Tanghus Olsen, John P Kress Intensive Care Medicine 2020 November 10
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Possible coexistence of MOG-IgG-associated disease and anti-Caspr2 antibody-associated autoimmune encephalitis: a first case report

Possible coexistence of MOG-IgG-associated disease and anti-Caspr2 antibody-associated autoimmune encephalitis: a first case report | AntiNMDA | Scoop.it
Myelin oligodendrocyte glycoprotein antibody-associated disease has been proposed as a separate inflammatory demyelinating disease of the central nervous system (CNS) since the discovery of pathogenic antibodies against myelin oligodendrocyte glycoprotein ...
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The Anti-NMDA Receptor Encephalitis Foundation Newsletter

The Anti-NMDA Receptor Encephalitis Foundation Newsletter | AntiNMDA | Scoop.it
On your Marks, Get Set, Register for the WORLD ENCEPHALITIS DAY CONFERENCE 2021 From...
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Autoimmune encephalitis: When your body attacks your brain, and people think you’re going mad

Autoimmune encephalitis: When your body attacks your brain, and people think you’re going mad | AntiNMDA | Scoop.it
Four PhD candidates from Monash University, who are already Doctors of the medical kind, are conducting research on a rare and debilitating neurological illness affecting the Australian population. It’s described as feeling like your brain is on fire.
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Characteristics of internalization of NMDA-type GluRs with antibodies to GluN1 and GluN2B - ScienceDirect

Characteristics of internalization of NMDA-type GluRs with antibodies to GluN1 and GluN2B - ScienceDirect | AntiNMDA | Scoop.it
To characterize internalization of NMDA-type glutamate receptors (GluRs) by antibodies to NMDA-type GluRs, we produced rabbit antibodies to N-terminal…
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Seizure-related 6 homolog like 2 autoimmunity | Neurology Neuroimmunology & Neuroinflammation

Seizure-related 6 homolog like 2 autoimmunity | Neurology Neuroimmunology & Neuroinflammation | AntiNMDA | Scoop.it
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Early clinical suspicion and treatment in a patient with anti-NMDA receptor encephalitis

Early clinical suspicion and treatment in a patient with anti-NMDA receptor encephalitis | AntiNMDA | Scoop.it
Anti-NMDA receptor encephalitis is a complicated disease associated with paraneoplastic syndromes and autoimmune conditions.This case report highlights the importance of early identification and reviews the common clinical manifestations, diagnostic studies, and treatment modalities for this potent...
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