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Normally Sharp, He Was Chronically Confused. What Was Going On? - The New York Times

Normally Sharp, He Was Chronically Confused. What Was Going On? - The New York Times | AntiNMDA | Scoop.it
He was getting lost driving home from work. And he was having strange spasms. What was the cause?
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Clinical spectrum of high-titre GAD65 antibodies | Journal of Neurology, Neurosurgery & Psychiatry

Neuro-inflammation Original research Clinical spectrum of high-titre GAD65 antibodies http://orcid.org/0000-0003-4860-0470Adrian Budhram1, http://orcid.org/0000-0003-4698-663XElia Sechi2,3, http://orcid.org/0000-0002-6661-2910Eoin P Flanagan2, Divyanshu Dubey4, Anastasia Zekeridou2, Shailee S Shah2, Avi Gadoth5, http://orcid.org/0000-0001-6212-1236Elie Naddaf2, http://orcid.org/0000-0001-6856-8143Andrew McKeon2, http://orcid.org/0000-0002-6140-5584Sean J Pittock6, Nicholas L Zalewski2 Clinical Neurological Sciences, Western University Schulich School of Medicine and Dentistry, London, Ontario, Canada Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA Department of Clinical and Experimental Medicine, University of Sassari, Sassari, Sassari, Italy Neurology and Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA Mayo Clinic, Rochester, Minnesota, USA Correspondence to Dr Nicholas L Zalewski, Neurology, Mayo Clinic Minnesota, Rochester, MN 55905, USA; zalewski.nicholas{at}mayo.edu Abstract Objective To determine clinical manifestations, immunotherapy responsiveness and outcomes of glutamic acid decarboxylase-65 (GAD65) neurological autoimmunity. Methods We identified 323 Mayo Clinic patients with high-titre (>20 nmol/L in serum) GAD65 antibodies out of 380 514 submitted anti-GAD65 samples (2003–2018). Patients classified as having GAD65 neurological autoimmunity after chart review were analysed to determine disease manifestations, immunotherapy responsiveness and predictors of poor outcome (modified Rankin score >2). Results On review, 108 patients were classified as not having GAD65 neurological autoimmunity and 3 patients had no more likely alternative diagnoses but atypical presentations (hyperkinetic movement disorders). Of remaining 212 patients with GAD65 neurological autoimmunity, median age at symptom onset was 46 years (range: 5–83 years); 163/212 (77%) were female. Stiff-person spectrum disorders (SPSD) (N=71), cerebellar ataxia (N=55), epilepsy (N=35) and limbic encephalitis (N=7) could occur either in isolation or as part of an overlap syndrome (N=44), and were designated core manifestations. Cognitive impairment (N=38), myelopathy (N=23) and brainstem dysfunction (N=22) were only reported as co-occurring phenomena, and were designated secondary manifestations. Sustained response to immunotherapy ranged from 5/20 (25%) in epilepsy to 32/44 (73%) in SPSD (p=0.002). Complete immunotherapy response occurred in 2/142 (1%). Cerebellar ataxia and serum GAD65 antibody titre >500 nmol/L predicted poor outcome. Interpretation High-titre GAD65 antibodies were suggestive of, but not pathognomonic for GAD65 neurological autoimmunity, which has discrete core and secondary manifestations. SPSD was most likely to respond to immunotherapy, while epilepsy was least immunotherapy responsive. Complete immunotherapy response was rare. Serum GAD65 antibody titre >500 nmol/L and cerebellar ataxia predicted poor outcome. Statistics from Altmetric.com View Full Text Footnotes Contributors AB designed/conceptualised the study, acquired/analysed the data, drafted the manuscript and composed the tables/figures. ES, EPF, DD, AZ, SSS, AG, EN and AM acquired/analysed the data, and revised the manuscript for intellectual content. SJP and NLZ designed/conceptualised the study, acquired/analyzed the data, revised the manuscript for intellectual content and supervised the study. Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors. Competing interests AB has no disclosures to report. ES has no disclosures to report. EPF is a site principal investigator in a randomised placebo-controlled clinical trial of Inebilizumab (A CD19 inhibitor) in neuromyelitis optica spectrum disorders funded by MedImmune/Viela Bio. He receives no personal compensation and just receives reimbursement for the research activities related to the trial. DD has a patent pending for Kelch-like protein 11 as a marker of neurological autoimmunity and has received research support from Grifols, Translational Research Innovation and Test Development Office and, Center for Clinical and Translational Science. DD has consulted for UCB and Astellas. All compensation for consulting activities is paid directly to Mayo Clinic. AZ has a patent pending for PDE10A-IgG as a biomarker of neurological autoimmunity. SS has no disclosures to report. AG has a patent pending for MAP1B IgG as a biomarker of neurological autoimmunity and small-cell lung cancer. EN has no disclosures to report. AM reports grants from Alexion, grants from Grifols, grants from Euroimmun, outside the submitted work; in addition, AM has a patent for Septin-5-IgG pending, a patent for PDE10A-IgG pending, a patent for MAP1B-IgG pending, and a patent for GFAP-IgG pending. SJP reports grants, personal fees and non-financial support from Alexion Pharmaceuticals; grants from Grifols, Autoimmune Encephalitis Alliance; grants, personal fees, non-financial support and other from MedImmune; SJP has a patent (patent #8889102) (application#12-678350) on neuromyelitis optica autoantibodies as a marker for neoplasia, and also a patent (patent #9891219B2) (application#12-573942) on methods for treating neuromyelitis optica (NMO) by administration of eculizumab to an individual that is aquaporin-4 (AQP4)-IgG autoantibody positive; SJP also has patents pending for the following IgGs as biomarkers of autoimmune neurological disorders (septin-5, Kelch-like protein 11, GFAP, PDE10A and MAP1B). NLZ has no disclosures to report. Patient consent for publication Not required. Ethics approval This study was approved by the institutional review board of the Mayo Clinic, Rochester, Minnesota. Provenance and peer review Not commissioned; externally peer reviewed. Data availability statement Data are available on reasonable request. Deidentified participant data will be made available to any qualified investigator on reasonable request directed to the corresponding author (NLZ). Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise. Request Permissions If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways. Copyright information: © Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ. Read the full text or download the PDF: Subscribe Log in
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Expert Alert: Encephalitis prevention another reason to receive COVID-19 vaccine – Mayo Clinic News Network

Expert Alert: Encephalitis prevention another reason to receive COVID-19 vaccine – Mayo Clinic News Network | AntiNMDA | Scoop.it
Expert Alert: Encephalitis prevention another reason to receive COVID-19 vaccine...
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Q&A: Early diagnosis critical in treating encephalitis due to COVID-19, other causes

Feb. 22 marks World Encephalitis Day, a day of global awareness started by the Encephalitis Society for individuals “who have been directly or indirectly affected by encephalitis,” which now includes patients with COVID-19.Healio Neurology spoke with Omar K.
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Seizures and memory impairment induced by patient-derived anti-N-methyl-D-aspartate receptor antibodies in mice are attenuated by anakinra, an interleukin-1 receptor antagonist

Seizures and memory impairment induced by patient-derived anti-N-methyl-D-aspartate receptor antibodies in mice are attenuated by anakinra, an interleukin-1 receptor antagonist | AntiNMDA | Scoop.it
Our evidence supports a role for IL-1 in the pathogenesis of seizures in anti-NMDAR encephalitis. These data are consistent with therapeutic effects of anakinra in other severe autoimmune and inflammatory seizure syndromes.
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Long-term Functional Outcomes and Relapse of Anti-NMDA Receptor Encephalitis | Neurology Neuroimmunology & Neuroinflammation

Long-term Functional Outcomes and Relapse of Anti-NMDA Receptor Encephalitis | Neurology Neuroimmunology & Neuroinflammation | AntiNMDA | Scoop.it
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Great article!

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Anti-NMDA receptor encephalitis with phenytoin toxicity: A diagnostic dilemma and management challenge Kumar A, Kumar N, Kumar A, Ghosh S - Indian J Anaesth

Anti-NMDA receptor encephalitis with phenytoin toxicity: A diagnostic dilemma and management challenge Kumar A, Kumar N, Kumar A, Ghosh S - Indian J Anaesth | AntiNMDA | Scoop.it
Indian Journal of Anaesthesia, Official publication of Indian Society of Anaesthesiologists...
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Association of Rituximab Use With Adverse Events in Children, Adolescents, and Young Adults | Adolescent Medicine | JAMA Network Open | JAMA Network

Association of Rituximab Use With Adverse Events in Children, Adolescents, and Young Adults | Adolescent Medicine | JAMA Network Open | JAMA Network | AntiNMDA | Scoop.it
This cohort study conducted at a large pediatric referral hospital assesses whether the use of rituximab for many diverse indications is associated with short-...
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Diagnostic Value of 18F-FDG PET/CT Versus MRI in the Setting of Antibody-Specific Autoimmune Encephalitis

Diagnostic Value of 18F-FDG PET/CT Versus MRI in the Setting of Antibody-Specific Autoimmune Encephalitis | AntiNMDA | Scoop.it
Diagnosis of autoimmune encephalitis presents some challenges in the clinical setting because of varied clinical presentations and delay in obtaining antibody panel results. We examined the role of neuroimaging in the setting of autoimmune encephalitides, ...
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Recent overview of patients with anti-N-methyl-D-aspartate receptor encephalitis using a national inpatient database in Japan

Recent overview of patients with anti-N-methyl-D-aspartate receptor encephalitis using a national inpatient database in Japan | AntiNMDA | Scoop.it
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Reader Response: Clinical Significance of Anti-NMDAR Concurrent With Glial or Neuronal Surface Antibodies

Reader Response: Clinical Significance of Anti-NMDAR Concurrent With Glial or Neuronal Surface Antibodies | AntiNMDA | Scoop.it
We welcome the study by Martinez-Hernandez et al.1 reporting antibody coexistence in anti-n-methyl-d-aspartate receptor (NMDA-R) encephalitis. The authors confirmed coexistence of aquaporin-4-IgG or myelin oligodendrocyte glycoprotein (MOG)-IgG as predictors of co-occurrence of anti-NMDA-R...
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Anti-N-methyl-D-aspartate receptor encephalitis associated with ovarian teratoma in Korea

Anti-N-methyl-D-aspartate receptor encephalitis associated with ovarian teratoma in Korea | AntiNMDA | Scoop.it
Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe autoimmune paraneoplastic syndrome associated with ovarian teratomas.Most patients develop neurologic symptoms, including psychosis, memory deficits, seizures, or abnormal movements, and experience abdominal pain related to ovarian...
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Paediatric multiple sclerosis and antibody-associated demyelination: clinical, imaging, and biological considerations for diagnosis and care

Paediatric multiple sclerosis and antibody-associated demyelination: clinical, imaging, and biological considerations for diagnosis and care | AntiNMDA | Scoop.it
The field of acquired CNS neuroimmune demyelination in children is transforming. Progress in assay development, refinement of diagnostic criteria, increased biological insights provided by advanced neuroimaging techniques, and high-level evidence for the therapeutic efficacy of biological agents...
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Antineuronal antibodies and epilepsy: treat the patient, not the lab | Journal of Neurology, Neurosurgery & Psychiatry

The study results implicate that starting immunosppressive treatment in new-onset epilepsy should be guided by clinics, not simply antibody presence Epilepsy affects about 70–80 million people worldwide; about one-third of patients cannot become seizure free. New diagnostic and therapeutic avenues to improve this situation are welcome. The impact of autoimmune phenomena on pathogenesis of some epilepsies increasingly gained attention as these mechanisms open the door for alternative medical treatments beyond antiseizure medications, that is, immunosuppressants. Thus, ‘autoimmune’ has become one of the six aetiologic categories of the new Intenational League Against Epilepsy classification of seizures and epilepsies. Numerous neuronal surface autoantibodies (NSAbs) identified in the past years cause autoimmune encephalitis (AE),1 often associated with severe seizures and status epilepticus. Additionally, the prevalence of NSAbs in patients with chronic epilepsies of unknown aetiology yielded a prevalence between 3% and 21%, but the question whether all epilepsy patients with NSAbs or only those with pharmacoresistant epilepsy (PRE) and/or additional signs of AE warrant immunosuppressants remained unresolved yet. A study looking at the presence of NSAbs in PRE found that 62% of patients responded to immunotherapy, and 34% even became seizure free, indicating that a trial may be justfied.2 But how does this result relate to patients with new-onset focal epilepsy (NFE)? The paper by Mc Ginty et al,3 tackles this issue by prospectively looking at those patients with NFE and a test positive for at least one NSAbs. The authors established an NSAbs prediction score based on clinical and paraclinical information and evaluated the value of immunotherapy in patients with NFE. About 10% of their cohort was NSAbs positive and 40% of them were diagnosed with AE. They identified six features which in combination were highly predictive for the presence of NSAbs, that is, age >54 years, ictal piloerection, self-reported lowered mood, MRI changes in the limbic system, the absence of ‘conventional’ epilepsy risk factors and intact attention. This ‘NSAbs-detecting’ Score compared better with the recently published ‘antibody prevalence in epilepsy and encephalopathy’ (APE2) Score4 in terms of forecasting AE, but worse in predicting presence of NSAbs. According to the present study (with an admittedly small sample of patients), immunotherapy could be omitted in those patients with NSAbs-positive new-onset epilepsy without signs or symptoms of AE. Conversely, the study also indicates that immunosuppressants are warranted in patients with even subtle AE. This is in line with another study where patients with AE even without NSAbs benefitted from immunosuppressants.5 The authors conclude that the administration of immunotherapy in NSAbs-positive patients should be guided by clinical signs for (subtle or obvious) AE and not only by NSAbs positivity per se. The study did not rely on cerebrospinal fluid data, probably leading to some missed cases of NSAbs positivity and AE. It is also interesting that 5/16 NSAbs positive, but AE-negative patients had mRS >0 and, thus, likely were pharmacoresistant, although this information was not exactly verifiable without follow-up phone interview. Statistically, this would exactly fit the one-third of patients basically becoming pharmacoresistant in chronic epilepsy of various aetiologies. Thus, future trials should test whether immunotherapy given to these patients would prevent pharmacoresistancy despite the fact that outcome without such treatment was mostly promising in this study.
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Cross-reactivity of a pathogenic autoantibody to a tumor antigen in GABAA receptor encephalitis | PNAS

Cross-reactivity of a pathogenic autoantibody to a tumor antigen in GABAA receptor encephalitis | PNAS | AntiNMDA | Scoop.it
RESEARCH ARTICLE Cross-reactivity of a pathogenic autoantibody to a tumor antigen in GABAA receptor encephalitis Simone M. Brändle, Manuela Cerina, View ORCID ProfileSusanne Weber, View ORCID ProfileKathrin Held, Amélie F. Menke, Carmen Alcalá, View ORCID ProfileDavid Gebert, View ORCID ProfileAlexander M. Herrmann, Hannah Pellkofer, View ORCID ProfileLisa Ann Gerdes, View ORCID ProfileStefan Bittner, View ORCID ProfileFrank Leypoldt, View ORCID ProfileBianca Teegen, View ORCID ProfileLars Komorowski, View ORCID ProfileTania Kümpfel, View ORCID ProfileReinhard Hohlfeld, View ORCID ProfileSven G. Meuth, View ORCID ProfileBonaventura Casanova, View ORCID ProfileNico Melzer, View ORCID ProfileEduardo Beltrán, and View ORCID ProfileKlaus Dornmair PNAS March 2, 2021 118 (9) e1916337118; https://doi.org/10.1073/pnas.1916337118 Edited by Lawrence Steinman, Stanford University School of Medicine, Stanford, CA, and approved January 11, 2021 (received for review June 19, 2020) Article Figures & SI Info & Metrics PDF Significance Antibodies recognizing the neuronal gamma-aminobutyric acid A receptor (GABAA-R) cause severe encephalitis by triggering internalization of the antibody–receptor complexes in inhibitory synapses, which leads to hyperexcitability and dysfunction of neuronal networks. From the cerebrospinal fluid of a patient with GABAA-R encephalitis we cloned a highly expressed antibody and showed that it binds the GABAA-R and influences signal transduction in neurons, explaining clinical symptoms. Using several experimental techniques, we confirmed that the antibody cross-reacts to an oncoprotein which is known to be involved in several malignancies. We showed that cross-reactivity to this oncoprotein may also be detected in two other GABAA-R patients, suggesting that such cross-reactivity is presumably a key event in the pathogenesis of GABAA-R encephalitis. Abstract Encephalitis associated with antibodies against the neuronal gamma-aminobutyric acid A receptor (GABAA-R) is a rare form of autoimmune encephalitis. The pathogenesis is still unknown but autoimmune mechanisms were surmised. Here we identified a strongly expanded B cell clone in the cerebrospinal fluid of a patient with GABAA-R encephalitis. We expressed the antibody produced by it and showed by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry that it recognizes the GABAA-R. Patch-clamp recordings revealed that it tones down inhibitory synaptic transmission and causes increased excitability of hippocampal CA1 pyramidal neurons. Thus, the antibody likely contributed to clinical disease symptoms. Hybridization to a protein array revealed the cross-reactive protein LIM-domain-only protein 5 (LMO5), which is related to cell-cycle regulation and tumor growth. We confirmed LMO5 recognition by immunoprecipitation and ELISA and showed that cerebrospinal fluid samples from two other patients with GABAA-R encephalitis also recognized LMO5. This suggests that cross-reactivity between GABAA-R and LMO5 is frequent in GABAA-R encephalitis and supports the hypothesis of a paraneoplastic etiology. Footnotes ↵1S.M.B., M.C., and S.W. contributed equally to this work. ↵2N.M., E.B., and K.D. contributed equally to this work. ↵3To whom correspondence may be addressed. Email: Klaus.Dornmair{at}med.uni-muenchen.de. Author contributions: R.H., S.G.M., B.C., N.M., E.B., and K.D. designed research; S.M.B., M.C., S.W., K.H., A.F.M., D.G., A.M.H., B.T., and E.B. performed research; C.A., H.P., L.A.G., S.B., F.L., L.K., T.K., B.C., and N.M. contributed new reagents/analytic tools; S.M.B., M.C., S.W., K.H., A.F.M., D.G., A.M.H., B.T., R.H., S.G.M., N.M., E.B., and K.D. analyzed data; and R.H., S.G.M., N.M., E.B., and K.D. wrote the paper. The authors declare no competing interest. This article is a PNAS Direct Submission. This article contains supporting information online at https://www.pnas.org/lookup/suppl/doi:10.1073/pnas.1916337118/-/DCSupplemental. Data Availability All study data are included in the article and/or SI Appendix. Published under the PNAS license. View Full Text References ↵ J. Dalmau, F. Graus, Antibody-mediated encephalitis. N. Engl. J. Med. 378, 840–851 (2018).OpenUrlCrossRefPubMed ↵ N. Melzer, S. G. Meuth, H. Wiendl, Paraneoplastic and non-paraneoplastic autoimmunity to neurons in the central nervous system. J. Neurol. 260, 1215–1233 (2013).OpenUrl ↵ C. Bost, O. Pascual, J. Honnorat, Autoimmune encephalitis in psychiatric institutions: Current perspectives. Neuropsychiatr. Dis. Treat. 12, 2775–2787 (2016).OpenUrlPubMed ↵ A. Vincent, C. G. Bien, S. R. Irani, P. Waters, Autoantibodies associated with diseases of the CNS: New developments and future challenges. Lancet Neurol. 10, 759–772 (2011).OpenUrlCrossRefPubMed ↵ M. H. van Coevorden-Hameete, E. de Graaff, M. J. Titulaer, C. C. Hoogenraad, P. A. Sillevis Smitt, Molecular and cellular mechanisms underlying anti-neuronal antibody mediated disorders of the central nervous system. Autoimmun. Rev. 13, 299–312 (2014).OpenUrlCrossRefPubMed ↵ M. J. Titulaer et al.; European Federation of Neurological Societies, Screening for tumours in paraneoplastic syndromes: Report of an EFNS task force. Eur. J. Neurol. 18, 19-e3 (2011).OpenUrlPubMed ↵ J. Dalmau, M. R. Rosenfeld, Paraneoplastic syndromes of the CNS. Lancet Neurol. 7, 327–340 (2008).OpenUrlCrossRefPubMed ↵ T. Ohkawa et al., Identification and characterization of GABA(A) receptor autoantibodies in autoimmune encephalitis. J. Neurosci. 34, 8151–8163 (2014). ↵ M. Petit-Pedrol et al., Encephalitis with refractory seizures, status epilepticus, and antibodies to the GABAA receptor: A case series, characterisation of the antigen, and analysis of the effects of antibodies. Lancet Neurol. 13, 276–286 (2014).OpenUrlCrossRefPubMed ↵ P. Pettingill et al., Antibodies to GABAA receptor α1 and γ2 subunits: Clinical and serologic characterization. Neurology 84, 1233–1241 (2015).OpenUrlCrossRefPubMed ↵ K. O’Connor et al., GABAA receptor autoimmunity: A multicenter experience. Neurol. Neuroimmunol. Neuroinflamm. 6, e552 (2019). ↵ C. Zhou et al., Altered cortical GABAA receptor composition, physiology, and endocytosis in a mouse model of a human genetic absence epilepsy syndrome. J. Biol. Chem. 288, 21458–21472 (2013). ↵ M. Spatola et al., Investigations in GABAA receptor antibody-associated encephalitis. Neurology 88, 1012–1020 (2017).OpenUrlPubMed ↵ C. Y. Guo, J. M. Gelfand, M. D. Geschwind, Anti-gamma-aminobutyric acid receptor type A encephalitis: A review. Curr. Opin. Neurol. 33, 372–380 (2020).OpenUrl ↵ M. M. Simabukuro et al., GABAA receptor and LGI1 antibody encephalitis in a patient with thymoma. Neurol. Neuroimmunol. Neuroinflamm. 2, e73 (2015). ↵ E. Lancaster, Encephalitis, severe seizures, and multifocal brain lesions: Recognizing autoimmunity to the GABAA receptor. Neurol. Neuroimmunol. Neuroinflamm. 6, e554 (2019). ↵ A. Bracher et al., An expanded parenchymal CD8+ T cell clone in GABAA receptor encephalitis. Ann. Clin. Transl. Neurol. 7, 239–244 (2020).OpenUrl ↵ J. M. Matthews, K. Lester, S. Joseph, D. J. Curtis, LIM-domain-only proteins in cancer. Nat. Rev. Cancer 13, 111–122 (2013).OpenUrlCrossRefPubMed ↵ Y. Midorikawa et al., Identification of genes associated with dedifferentiation of hepatocellular carcinoma with expression profiling analysis. Jpn. J. Cancer Res. 93, 636–643 (2002).OpenUrlCrossRef ↵ Z. Hu et al., The molecular portraits of breast tumors are conserved across microarray platforms. BMC Genomics 7, 96 (2006).OpenUrlCrossRefPubMed ↵ C. Hoffmann et al., CRP2, a new invadopodia actin bundling factor critically promotes breast cancer cell invasion and metastasis. Oncotarget 7, 13688–13705 (2016).OpenUrl ↵ B. Schlick et al., Serum autoantibodies in chronic prostate inflammation in prostate cancer patients. PLoS One 11, e0147739 (2016).OpenUrl ↵ C. Hoffmann et al., Hypoxia promotes breast cancer cell invasion through HIF-1α-mediated up-regulation of the invadopodial actin bundling protein CSRP2. Sci. Rep. 8, 10191 (2018).OpenUrlCrossRefPubMed ↵ S. J. Wang et al., Cysteine and glycine-rich protein 2 (CSRP2) transcript levels correlate with leukemia relapse and leukemia-free survival in adults with B-cell acute lymphoblastic leukemia and normal cytogenetics. Oncotarget 8, 35984–36000 (2017).OpenUrl ↵ S. M. Brändle et al., Distinct oligoclonal band antibodies in multiple sclerosis recognize ubiquitous self-proteins. Proc. Natl. Acad. Sci. U.S.A. 113, 7864–7869 (2016). ↵ H. B. Michelson, R. K. Wong, Excitatory synaptic responses mediated by GABAA receptors in the hippocampus. Science 253, 1420–1423 (1991). ↵ S. Schuster et al., Fatal PCR-negative herpes simplex virus-1 encephalitis with GABAA receptor antibodies. Neurol. Neuroimmunol. Neuroinflamm. 6, e624 (2019). ↵ S. Sala, C. Ampe, An emerging link between LIM domain proteins and nuclear receptors. Cell. Mol. Life Sci. 75, 1959–1971 (2018).OpenUrlCrossRef ↵ B. Obermeier et al., Matching of oligoclonal immunoglobulin transcriptomes and proteomes of cerebrospinal fluid in multiple sclerosis. Nat Med. 14, 688–693 (2008).OpenUrlCrossRefPubMed ↵ M. Cerina et al., Thalamic Kv 7 channels: Pharmacological properties and activity control during noxious signal processing. Br. J. Pharmacol. 172, 3126–3140 (2015).OpenUrl ↵ P. Blaesse et al., μ-Opioid receptor-mediated inhibition of Intercalated neurons and effect on synaptic transmission to the central amygdala. J. Neurosci. 35, 7317–7325 (2015). ↵ S. M. Brändle, “Analysis of oligoclonal band antibodies from patients with neurological diseases,” PhD thesis, Ludwig Maximilians University of Munich, Munich, Germany (2016). Log in using your username and password Username * Password * Log in Forgot your user name or password? Log in through your institution You may be able to gain access using your login credentials for your institution. Contact your library if you do not have a username and password. If your organization uses OpenAthens, you can log in using your OpenAthens username and password. To check if your institution is supported, please see this list. Contact your library for more details. Purchase access You may purchase access to this article. This will require you to create an account if you don't already have one. Subscribers, for more details, please visit our Subscriptions FAQ. Please click here to log into the PNAS submission website. Previous Next Share Sign up for the PNAS Highlights newsletter to get in-depth stories of science sent to your inbox twice a month: Sign up for Article Alerts Sign up ARTICLE CLASSIFICATIONS Biological SciencesImmunology and Inflammation JUMP TO SECTION YOU MAY ALSO BE INTERESTED IN Scientists should pursue a strategic approach to research, focusing on the accumulation of evidence via designed sequences of studies. Image credit: Dave Cutler (artist). Despite myriad challenges, clinicians see room for progress. 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Expert Alert: Encephalitis prevention another reason to receive COVID-19 vaccine

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Patients with COVID-19 are at risk for neurologic complications, including encephalitis, or inflammation of the brain."Encephalitis cases have been report...
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Distinguishing between two very similar pediatric brain conditions

Distinguishing between two very similar pediatric brain conditions | AntiNMDA | Scoop.it
Slight differences in clinical features can help physicians distinguish between two rare but similar forms of autoimmune brain inflammation in children, a new study by UT Southwestern scientists suggests.
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Relationship Between Serum NMDA Receptor Antibodies and Response to Antipsychotic Treatment in First-Episode Psychosis - UCL Discovery

Relationship Between Serum NMDA Receptor Antibodies and Response to Antipsychotic Treatment in First-Episode Psychosis - UCL Discovery | AntiNMDA | Scoop.it
UCL Discovery is UCL's open access repository, showcasing and providing access to UCL research outputs from all UCL disciplines.
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Treatment of Movement Disorder Emergencies in Autoimmune Encephalitis in the Neurosciences ICU

Treatment of Movement Disorder Emergencies in Autoimmune Encephalitis in the Neurosciences ICU | AntiNMDA | Scoop.it
Immune response against neuronal and glial cell surface and cytosolic antigens is an important cause of encephalitis. It may be triggered by activation of the immune system in response to an infection (para-infectious), cancer (paraneoplastic), or due to a patient's tendency toward autoimmunity.
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Bortezomib for treatment of anti-NMDA receptor encephalitis in a pediatric patient refractory to conventional therapy

Bortezomib for treatment of anti-NMDA receptor encephalitis in a pediatric patient refractory to conventional therapy | AntiNMDA | Scoop.it
A 5-year-old female with anti-NMDA receptor encephalitis was successfully treated with bortezomib after having shown no clinical improvement during treatment with IVIG, high-dose methylprednisolone, plasmapheresis, and rituximab.
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Searching for autoimmune encephalitis: Beware of normal CSF - ScienceDirect

Searching for autoimmune encephalitis: Beware of normal CSF - ScienceDirect | AntiNMDA | Scoop.it
To determine the prevalence of cerebrospinal fluid (CSF) markers associated with inflammation (i.e., elevated white blood cell count, protein concentr…...
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Delirious Mania as a Neuropsychiatric Presentation in Patients With Anti–N-methyl-D-aspartate Receptor Encephalitis - ScienceDirect

Delirious Mania as a Neuropsychiatric Presentation in Patients With Anti–N-methyl-D-aspartate Receptor Encephalitis - ScienceDirect | AntiNMDA | Scoop.it
Psychosomatics Volume 61, Issue 1, January–February 2020, Pages 64-69 Case Report Delirious Mania as a Neuropsychiatric Presentation in Patients With Anti–N-methyl-D-aspartate Receptor Encephalitis Author links open overlay panel Show more Cite View full text © 2019 Academy of Consultation-Liaison Psychiatry. Published by Elsevier Inc. All rights reserved.
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Clinical features of paediatric and adult autoimmune encephalitis: A multicenter sample

Clinical features of paediatric and adult autoimmune encephalitis: A multicenter sample | AntiNMDA | Scoop.it
Autoimmune encephalitis (AE) is a heterogeneous class of inflammatory diseases of
the brain that can present with a wide spectrum of neuropsychiatric symptoms. Patients
may be negative for CSF anti-neuronal antibodies, which can make the diagnosis of
AE challenging.
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Editors' Note: Clinical Significance of Anti-NMDAR Concurrent With Glial or Neuronal Surface Antibodies | Neurology

Editors' Note: Clinical Significance of Anti-NMDAR Concurrent With Glial or Neuronal Surface Antibodies | Neurology | AntiNMDA | Scoop.it
SHARE January 26, 2021; 96 (4) DISPUTES & DEBATES: EDITORS' CHOICE Editors' Note: Clinical Significance of Anti-NMDAR Concurrent With Glial or Neuronal Surface Antibodies Ariane Lewis, Steven Galetta First published January 25, 2021, DOI: https://doi.org/10.1212/WNL.0000000000011358 FULL PDF CITATION PERMISSIONS MAKE COMMENT SEE COMMENTS Downloads0 This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased. In “Clinical Significance of Anti-NMDAR Concurrent With Glial or Neuronal Surface Antibodies,” Martinez-Hernandez et al. reported that between 4% and 7.5% of patients with anti-NMDAR encephalitis have concurrent glial or neuronal surface antibodies (glial-Ab or NS-Ab). Although they found that the presence of myelin oligodendrocyte glycoprotein (MOG) or aquaporin 4 antibodies was associated with demyelinating disorders and NS-Ab was associated with medial temporal or subcortical MRI findings, a positive glial fibrillary acidic protein (GFAP) antibody was nonspecific. McKeon et al. suggested the coexistence of GFAP antibodies and their significance may have been underreported in this study as both serum and CSF testing can be imperfect and that a phenotypic clinical-radiographic presentation associated with this antibody—a steroid-responsive meningoencephalitis with a predilection for the midbrain, cerebellar white matter, hippocampus, and cortex—may have been missed. Martinez-Hernandez et al. responded that McKeon et al. (1) misunderstood the frequency of NMDAR-Ab and GFAP-Ab co-occurrence in their cohort and (2) mischaracterized the specificity of GFAP-Ab. Lancaster reinforced Martinez-Hernandez et al.’s findings, noting that clinicians must be aware that patients with anti-NMDAR encephalitis can have multiple antibodies, which may impact presentation and prognosis. Dalmau and Martinez-Hernandez further commented that patients with NMDAR-Ab who have an atypical presentation of anti-NMDAR encephalitis should prompt consideration of the possibility that the presence of NMDAR-Ab was a false positive or that there could be concurrent antibodies but that the conclusion that any particular clinical or radiologic findings are associated with any particular antibody can only be made after careful evaluation for disease specificity. In “Clinical Significance of Anti-NMDAR Concurrent With Glial or Neuronal Surface Antibodies,” Martinez-Hernandez et al. reported that between 4% and 7.5% of patients with anti-NMDAR encephalitis have concurrent glial or neuronal surface antibodies (glial-Ab or NS-Ab). Although they found that the presence of myelin oligodendrocyte glycoprotein (MOG) or aquaporin 4 antibodies was associated with demyelinating disorders and NS-Ab was associated with medial temporal or subcortical MRI findings, a positive glial fibrillary acidic protein (GFAP) antibody was nonspecific. McKeon et al. suggested the coexistence of GFAP antibodies and their significance may have been underreported in this study as both serum and CSF testing can be imperfect and that a phenotypic clinical-radiographic presentation associated with this antibody—a steroid-responsive meningoencephalitis with a predilection for the midbrain, cerebellar white matter, hippocampus, and cortex—may have been missed. Martinez-Hernandez et al. responded that McKeon et al. (1) misunderstood the frequency of NMDAR-Ab and GFAP-Ab co-occurrence in their cohort and (2) mischaracterized the specificity of GFAP-Ab. Lancaster reinforced Martinez-Hernandez et al.’s findings, noting that clinicians must be aware that patients with anti-NMDAR encephalitis can have multiple antibodies, which may impact presentation and prognosis. Dalmau and Martinez-Hernandez further commented that patients with NMDAR-Ab who have an atypical presentation of anti-NMDAR encephalitis should prompt consideration of the possibility that the presence of NMDAR-Ab was a false positive or that there could be concurrent antibodies but that the conclusion that any particular clinical or radiologic findings are associated with any particular antibody can only be made after careful evaluation for disease specificity. Footnotes Author disclosures are available upon request (journal{at}neurology.org). See letter See letter See response © 2021 American Academy of Neurology View Full Text AAN Members We have changed the login procedure to improve access between AAN.com and the Neurology journals. If you are experiencing issues, please log out of AAN.com and clear history and cookies. (For instructions by browser, please click the instruction pages below). After clearing, choose preferred Journal and select login for AAN Members. You will be redirected to a login page where you can log in with your AAN ID number and password. When you are returned to the Journal, your name should appear at the top right of the page. Google Safari Microsoft Edge Firefox CLICK HERE TO LOGIN AAN Non-Member Subscribers CLICK HERE TO LOGIN Purchase access For assistance, please contact: AAN Members (800) 879-1960 or (612) 928-6000 (International) Non-AAN Member subscribers (800) 638-3030 or (301) 223-2300 option 3, select 1 (international) Sign Up Information on how to subscribe to Neurology and Neurology: Clinical Practice can be found here  Purchase Individual access to articles is available through the Add to Cart option on the article page.  Access for 1 day (from the computer you are currently using) is US$ 39.00.  Pay-per-view content is for the use of the payee only, and content may not be further distributed by print or electronic means.  The payee may view, download, and/or print the article for his/her personal, scholarly, research, and educational use.  Distributing copies (electronic or otherwise) of the article is not allowed. 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From brain to behaviour

From brain to behaviour | AntiNMDA | Scoop.it
Each month Nature Communications’ editors highlight new Articles they see as particularly interesting or important in the area of neuroscience research.
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Seizures in autoimmune encephalitis—A systematic review and quantitative synthesis - Yeshokumar - - Epilepsia

Seizures in autoimmune encephalitis—A systematic review and quantitative synthesis - Yeshokumar - - Epilepsia | AntiNMDA | Scoop.it
Abstract Objective This study aimed to evaluate the proportion of patients with seizures and electroencephalography (EEG) abnormalities in autoimmune encephalitis (AE) and its most common subtypes....
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