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Cerebrospinal Fluid Findings in Patients With Autoimmune Encephalitis-A Systematic Analysis | Read by QxMD

Cerebrospinal Fluid Findings in Patients With Autoimmune Encephalitis-A Systematic Analysis | Read by QxMD | AntiNMDA | Scoop.it
Cerebrospinal Fluid Findings in Patients With Autoimmune Encephalitis-A Systematic Analysis Tetyana Blinder, Jan Lewerenz Frontiers in Neurology 2019, 10: 804 Autoimmune encephalitides (AIE) comprise a group of inflammatory diseases of the central nervous system (CNS), which can be further characterized by the presence of different antineuronal antibodies. Recently, a clinical approach for diagnostic criteria for the suspected diagnosis of AIE as well as definitive AIE were proposed. These are intended to guide physicians when to order the antineuronal antibody testing and/or facilitate early diagnosis even prior to the availability of the specific disease-confirming test results to facilitate prompt treatment. These diagnostic criteria also include the results of basic cerebrospinal fluid (CSF) analysis. However, the different antibody-defined AIE subtypes might be highly distinct with regard to their immune pathophysiology, e.g., the pre-dominance of specific IgG subclasses, IgG1, or IgG4, or frequency of paraneoplastic compared to idiopathic origin. Thus, it is conceivable that the results of basic CSF analysis might also be very different. However, this has not been explored systematically. Here, we systematically reviewed the literature about the 10 most important AIE subtypes, AIE with antibodies against NMDA, AMPA, glycine, GABAA , and GABAB receptors as well as DPPX, CASPR2, LGI1, IgLON5, or glutamate decarboxylase (GAD), with respect to the reported basic CSF findings comprising CSF leukocyte count, total protein, and the presence of oligoclonal bands (OCB) restricted to the CSF as a sensitive measure for intrathecal IgG synthesis. Our results indicate that these basic CSF findings are profoundly different among the 10 different AIE subtypes. Whereas, AIEs with antibodies against NMDA, GABAB , and AMPA receptors as well as DPPX show rather frequent inflammatory CSF changes, in AIEs with either CASPR2, LGI1, GABAA , or glycine receptor antibodies CSF findings were mostly normal. Two subtypes, AIEs defined by either GAD, or IgLON5 antibodies, did not fit into this general pattern. In AIE with GAD antibodies, positive OCBs in the absence of other changes were typical, while the CSF in IgLON5 antibody-positive AIE was characterized by elevated protein. Comments You need to log in or sign up for an account to be able to comment. No comments yet, be the first to post one! Related Papers
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Encephalitis411 to host Encephalitis Event in the Dallas, Texas area, 21 September 2019

Encephalitis411 to host Encephalitis Event in the Dallas, Texas area, 21 September 2019 | AntiNMDA | Scoop.it
We are pleased to share with you the details of an event that will take place in the Dallas, Texas area on September 21, 2019.
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Long‐term cognitive and neuropsychiatric outcomes in patients with anti‐NMDAR encephalitis - Liu - - Acta Neurologica Scandinavica

Long‐term cognitive and neuropsychiatric outcomes in patients with anti‐NMDAR encephalitis - Liu - - Acta Neurologica Scandinavica | AntiNMDA | Scoop.it
Abstract Objectives To evaluate the long‐term cognitive or neuropsychiatric outcomes and potential risk factors associated with prolonged cognitive deficits or neuropsychiatric symptoms in patients...
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Presence of cerebrospinal fluid antibodies associated with autoimmune encephalitis of humans in dogs with neurologic disease. - PubMed - NCBI

Presence of cerebrospinal fluid antibodies associated with autoimmune encephalitis of humans in dogs with neurologic disease. - PubMed - NCBI | AntiNMDA | Scoop.it
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
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Plasma cell depletion with bortezomib in the treatment of refractory N-methyl-d-aspartate (NMDA) receptor antibody encephalitis. Rational developments in neuroimmunological treatment - UCL Discovery

Plasma cell depletion with bortezomib in the treatment of refractory N-methyl-d-aspartate (NMDA) receptor antibody encephalitis. Rational developments in neuroimmunological treatment - 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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Encephalitis - Autoimmune Encephalitis with Dr Bo Sun - My Brain and Medicine 2019

Dr Bo Sun gives a presentation on autoimmune encephalitis - it's causes and diagnosis, at the Royal Society of Medicine, April 29th, 2019. He also discusses ...
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Ketamine use in refractory status epilepticus associated with anti-NMDA receptor antibody encephalitis | Read by QxMD

Ketamine use in refractory status epilepticus associated with anti-NMDA receptor antibody encephalitis | Read by QxMD | AntiNMDA | Scoop.it
Purpose: Anti- N -methyl-D-aspartate receptor encephalitis (anti-NMDAr encephalitis) is an auto-immune disorder associated with the production of antibodies against NR1 and NR2 sub units of the NMDA receptor. Seizures in this population are reported in up to 50% of cases with status epilepticus being reported in 25% of cases, refractory status epilepticus in 13.8% of cases and super-refractory status epilepticus in 10.2% of cases. Treatment of refractory epileptic activity in this population is not uniform and heterogeneous. Methods: We present three cases of super refractory status epilepticus in patients with anti-NMDAr encephalitis treated successfully with ketamine, a noncompetitive NMDA receptor antagonist. All patients had failed to improve clinically on multiple anti-convulsants and immunotherapy prior to initiation of ketamine therapy. Results: In all three cases, administration of a load followed by maintenance infusion (0.05 mg/kg/min infusion) of ketamine yielded clinical and/or electrographic seizure cessation in less than 48 h. Patients were treated for a heterogeneous duration although ultimately, epilepsy outcomes were favorable from a seizure freedom standpoint. Earlier treatments with ketamine were associated with better epilepsy outcomes in this case series. Conclusions: Ketamine may be a useful adjunct treatment in super-refractory status epilepticus in patients with NMDAr encephalitis.
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A Case of HIV Seroconversion Presenting Similarly to Anti- N-methyl- d-aspartate Receptor Encephalitis

A Case of HIV Seroconversion Presenting Similarly to Anti- N-methyl- d-aspartate Receptor Encephalitis | AntiNMDA | Scoop.it
1. Herman ST, Abend NS, Bleck TP, et al. Consensus statement on continuous EEG in critically ill adults and children, part I: indications. J Clin Neurophysiol. 2015;32:87–95. CrossRefGoogle Scholar 2. Vitaliani R, Mason W, Ances B, Zwerdling T, Jiang Z, Dalmau J. Paraneoplastic encephalitis, psychiatric symptoms, and hypoventilation in ovarian teratoma. Ann Neurol. 2005;58:594–604. CrossRefGoogle Scholar 3. Dalmau J, Tuzun E, Wu HY, et al. Paraneoplastic anti-N-methyl-d-aspartate receptor encephalitis associated with ovarian teratoma. Ann Neurol. 2007;61:25–36. CrossRefGoogle Scholar 4. Gordon-Lipkin E, Yeshokumar AK, Saylor D, Arenivas A, Probasco JC. Comparative outcomes in children and adults with anti-N-methyl-d-aspartate (anti-NMDA) receptor encephalitis. J Child Neurol. 2017;32:930–5. CrossRefGoogle Scholar 5. Guasp M, Dalmau J. Encephalitis associated with antibodies against the NMDA receptor. Med Clin (Barc). 2018;151:71–9. CrossRefGoogle Scholar 6. Titulaer MJ, McCracken L, Gabilondo I, et al. Treatment and prognostic factors for long-term outcome in patients with anti-NMDA receptor encephalitis: an observational cohort study. Lancet Neurol. 2013;12:157–65. CrossRefGoogle Scholar 7. Schmitt SE, Pargeon K, Frechette ES, Hirsch LJ, Dalmau J, Friedman D. Extreme delta brush: a unique EEG pattern in adults with anti-NMDA receptor encephalitis. Neurology. 2012;79:1094–100. CrossRefGoogle Scholar 8. Wang J, Wang K, Wu D, Liang H, Zheng X, Luo B. Extreme delta brush guides to the diagnosis of anti-NMDAR encephalitis. J Neurol Sci. 2015;353:81–3. CrossRefGoogle Scholar 9. Foff EP, Taplinger D, Suski J, Lopes MB, Quigg M. EEG findings may serve as a potential biomarker for anti-NMDA receptor encephalitis. Clin EEG Neurosci. 2017;48:48–53. CrossRefGoogle Scholar 10. Dalmau J, Lancaster E, Martinez-Hernandez E, Rosenfeld MR, Balice-Gordon R. Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis. Lancet Neurol. 2011;10:63–74. CrossRefGoogle Scholar 11. Hinson HE, Takahashi C, Altowaijri G, Baguley IJ, Bourdette D. Anti-NMDA receptor encephalitis with paroxysmal sympathetic hyperactivity: an under-recognized association? Clin Auton Res. 2013;23:109–11. CrossRefGoogle Scholar 12. Liu X, Yan B, Wang R, et al. Seizure outcomes in patients with anti-NMDAR encephalitis: a follow-up study. Epilepsia. 2017;58:2104–11. CrossRefGoogle Scholar 13. Maneta E, Garcia G. Psychiatric manifestations of anti-NMDA receptor encephalitis: neurobiological underpinnings and differential diagnostic implications. Psychosomatics. 2014;55:37–44. CrossRefGoogle Scholar 14. Mohammad SS, Dale RC. EEG background activity and extreme delta brush in children with anti-NMDAR encephalitis. Eur J Paediatr Neurol. 2018;22:207–8. CrossRefGoogle Scholar 15. Castellano J, Glover R, Robinson J. Extreme delta brush in NMDA receptor encephalitis. Neurohospitalist. 2017;7:NP3–4. CrossRefGoogle Scholar 16. Armangue T, Titulaer MJ, Malaga I, et al. Pediatric anti-N-methyl-d-aspartate receptor encephalitis-clinical analysis and novel findings in a series of 20 patients. J Pediatr. 2013;162(850–6):e2. Google Scholar 17. Yildirim M, Konuskan B, Yalnizoglu D, Topaloglu H, Erol I, Anlar B. Electroencephalographic findings in anti-N-methyl-d-aspartate receptor encephalitis in children: a series of 12 patients. Epilepsy Behav. 2018;78:118–23. CrossRefGoogle Scholar 18. Zhang Y, Liu G, Jiang MD, Li LP, Su YY. Analysis of electroencephalogram characteristics of anti-NMDA receptor encephalitis patients in China. Clin Neurophysiol. 2017;128:1227–33. CrossRefGoogle Scholar 19. Casciato S, Gambardella S, Mascia A, et al. Severe and rapidly-progressive Lafora disease associated with NHLRC1 mutation: a case report. Int J Neurosci. 2017;127:1150–3. CrossRefGoogle Scholar 20. Theroux LM, Goodkin HP, Heinan KC, Quigg M, Brenton JN. Extreme delta brush and distinctive imaging in a pediatric patient with autoimmune GFAP astrocytopathy. Mult Scler Relat Disord. 2018;26:121–3. CrossRefGoogle Scholar 21. Schmidt LS, Kjaer TW, Schmiegelow K, Born AP. EEG with extreme delta brush in young female with methotrexate neurotoxicity supports NMDA receptor involvement. Eur J Paediatr Neurol. 2017;21:795–7. CrossRefGoogle Scholar 22. Farias-Moeller R, Bartolini L, Staso K, Schreiber JM, Carpenter JL. Early ictal and interictal patterns in FIRES: the sparks before the blaze. Epilepsia. 2017;58:1340–8. CrossRefGoogle Scholar 23. Baykan B, Gungor Tuncer O, Vanli-Yavuz EN, et al. Delta brush pattern is not unique to NMDAR encephalitis: evaluation of two independent long-term EEG cohorts. Clin EEG Neurosci. 2018;49:278–84. CrossRefGoogle Scholar 24. Graus F, Titulaer MJ, Balu R, et al. A clinical approach to diagnosis of autoimmune encephalitis. Lancet Neurol. 2016;15:391–404. CrossRefGoogle Scholar 25. Kahn JO, Walker BD. Acute human immunodeficiency virus type 1 infection. N Engl J Med. 1998;339:33–9. CrossRefGoogle Scholar 26. Hogan C, Wilkins E. Neurological complications in HIV. Clin Med (Lond). 2011;11:571–5. CrossRefGoogle Scholar 27. Zhang J, Liu J, Katafiasz B, Fox H, Xiong H. HIV-1 gp120-induced axonal injury detected by accumulation of beta-amyloid precursor protein in adult rat corpus callosum. J Neuroimmune Pharmacol. 2011;6:650–7. CrossRefGoogle Scholar 28. Hoefer MM, Sanchez AB, Maung R, et al. Combination of methamphetamine and HIV-1 gp120 causes distinct long-term alterations of behavior, gene expression, and injury in the central nervous system. Exp Neurol. 2015;263:221–34. CrossRefGoogle Scholar 29. Kaul M, Garden GA, Lipton SA. Pathways to neuronal injury and apoptosis in HIV-associated dementia. Nature. 2001;410:988–94. CrossRefGoogle Scholar 30. Zhou Y, Liu J, Xiong H. HIV-1 glycoprotein 120 enhancement of N-methyl-d-aspartate NMDA receptor-mediated excitatory postsynaptic currents: implications for HIV-1-associated neural injury. J Neuroimmune Pharmacol. 2017;12:314–26. CrossRefGoogle Scholar 31. O’Donnell LA, Agrawal A, Jordan-Sciutto KL, Dichter MA, Lynch DR, Kolson DL. Human immunodeficiency virus (HIV)-induced neurotoxicity: roles for the NMDA receptor subtypes. J Neurosci. 2006;26:981–90. CrossRefGoogle Scholar
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An anti-NMDA receptor encephalitis mimicking an HIV encephalitis. - PubMed - NCBI

An anti-NMDA receptor encephalitis mimicking an HIV encephalitis. - PubMed - NCBI | AntiNMDA | Scoop.it
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
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Rituximab-associated Hypogammaglobulinemia in pediatric patients with autoimmune diseases | Pediatric Rheumatology | Full Text

Rituximab-associated Hypogammaglobulinemia in pediatric patients with autoimmune diseases | Pediatric Rheumatology | Full Text | AntiNMDA | Scoop.it
Despite the increased use of rituximab in treating pediatric patients with autoimmune diseases in the last decade, there are limited data on rituximab safety in those subjects who have a developing immune system.
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Evaluation of seizure treatment in anti-LGI1, anti-NMDAR, and anti-GABABR encephalitis

Evaluation of seizure treatment in anti-LGI1, anti-NMDAR, and anti-GABABR encephalitis | AntiNMDA | Scoop.it
This nationwide cohort study evaluates seizure responses to immunotherapy and antiepileptic drugs (AEDs) in patients with anti-leucine-rich glioma-inactivated 1 (LGI1), anti-NMDA receptor (NMDAR), and anti-gamma-aminobutyric-acid B receptor (GABA[B] R) ...
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Serial Brain Positron Emission Tomography Fused to Magnetic Resonance Imaging in Post-Infectious and Autoantibody-Associated Autoimmune Encephalitis

Serial Brain Positron Emission Tomography Fused to Magnetic Resonance Imaging in Post-Infectious and Autoantibody-Associated Autoimmune Encephalitis | AntiNMDA | Scoop.it
Serial positron emission tomography fused to magnetic resonance imaging showed progression of GAD65 autoimmune encephalitis.
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Ketamine use in refractory status epilepticus associated with anti-NMDA receptor antibody encephalitis. - PubMed - NCBI

Ketamine use in refractory status epilepticus associated with anti-NMDA receptor antibody encephalitis. - PubMed - NCBI | AntiNMDA | Scoop.it
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
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Encephalitis411 to host Encephalitis Event in the Dallas, Texas area, 21 September 2019

Encephalitis411 to host Encephalitis Event in the Dallas, Texas area, 21 September 2019 | AntiNMDA | Scoop.it
We are pleased to share with you the details of an event that will take place in the Dallas, Texas area on September 21, 2019.
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Theresa Mobilio on being an anti-NMDA Survivor – Podcast with host and producer Emily Krauser

Theresa Mobilio on being an anti-NMDA Survivor – Podcast with host and producer Emily Krauser | AntiNMDA | Scoop.it
Over the past 10 years, anti-NMDA receptor encephalitis survivors and /or caregivers have played an important role in raising the profile and awareness of the ...Read More...
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Toll-like receptor 3 deficiency in autoimmune encephalitis post–herpes simplex encephalitis | Neurology Neuroimmunology & Neuroinflammation

Toll-like receptor 3 deficiency in autoimmune encephalitis post–herpes simplex encephalitis | Neurology Neuroimmunology & Neuroinflammation | AntiNMDA | Scoop.it
The Toll-like receptor 3 (TLR3) pathway is a key component of the innate immunity that prevents replication of viruses in the CNS. Inborn errors of this pathway (TLR3-pathway deficiency), which includes defects in the genes TLR3, UNC93B1, TRIF, TRAF3, TBK1 and IRF3, occur in 10% of patients with herpes simplex encephalitis (HSE),1,2 and about 66% of these patients develop relapses of HSE.1 A recent study showed that 27% of patients with HSE develop autoimmune encephalitis (AE) in the weeks or months ensuing the infection.3 It is unknown whether TLR3-pathway deficient patients can also develop AE post-HSE. Here we report a patient with TLR3-pathway deficiency who developed HSE and a relapse of the viral infection followed by AE post-HSE, highlighting the fact that TLR3-pathway deficient patients should be carefully followed for both HSE relapses and AE. Case A 6-year-old healthy Caucasian girl, with a family history of maternal grandfather with recurrent herpetic keratitis, developed acute-onset headache, fever, decreased level of consciousness, aphasia, and right hemiparesis. Brain MRI showed bilateral hemorrhagic temporal lesions leading to suspect HSE. Signs of cranial hypertension precluded CSF studies; however, a positive herpes simplex virus 1 (HSV-1) PCR was obtained in the blood samples. IV acyclovir resulted in symptom improvement, and 3 weeks later the patient was discharged home with residual aphasia. Five months later, she was readmitted with severe headache and decreased level of consciousness. Brain CT showed new hemorrhagic temporal lesions. She required urgent decompressive craniectomy, and a brain tissue sample was HSV-1 PCR positive. Genetic studies showed that the patient and the mother carried a heterozygous missense mutation p.Glu110Lys (c.328G>A) in exon 2 of the gene TLR3 (NM_003265.2) (figure, A and B). Such mutation shows a very low allelic frequency (0.00082%, 1/121,316). Functional studies on patient's fibroblasts (figure, C) and monocyte-derived dendritic cells showed a decrease in TLR3-mediated activation (methods in appendix e-1, links.lww.com/NXI/A141). The patient received a new 21-day course of IV acyclovir followed by oral valganciclovir. Figure Genetic, functional, and immunologic studies in a 6-year-old child with TLR3-pathway deficiency who developed HSE, and a relapse of the viral infection followed by AE post-HSE (A and B) Genetic studies identified a missense heterozygous mutation p.Glu110Lys (c.328G>A) in exon 2 of the TLR3 gene (NM_003265.2) in the patient and her mother (who was asymptomatic). The patient's grandfather had history of severe recurrent herpetic keratitis but at the time our patient was studied, he was deceased, and no genetic studies were available. (C) IFN-β production by fibroblasts of the patient (red squares) and a healthy control (black dots) in 2 independent experiments after 24 hours stimulation with 2 different TLR3 agonists: Poly(I:C) or Poly(I:C) LMW; stimulation with its own culture media was used as negative control (negative). IL-6 production by TLR3-agonists stimulated MDDCs was also decreased in the patient compared with a healthy control in 2 independent experiments (data not shown). (D) Rat brain immunostaining with CSF of the patient (upper panel) indicating the presence of antibodies against neuronal surface antigens, compared with that of a healthy control individual (lower panel). Scale bar = 2,000 μm. AE = autoimmune encephalitis; HSE = herpes simplex encephalitis; IFN-β = interferon-beta; LMW = low molecular weight; MDDC = monocyte-derived dendritic cell; Poly(I:C) = polyinosinic-polycytidylic acid; TLR3 = Toll-like receptor 3. One year later, 17 months after the initial episode of HSE, she developed behavioral changes characterized by aggressivity and paranoid thoughts. CSF studies showed pleocytosis (15 cells/μL) and elevated protein concentration (100 mg/dL) but were HSV-1 PCR negative. CSF immunochemistry studies on rat brain tissue (figure, D, upper panel) and cultured live neurons showed strong reactivity revealing the presence of neuronal antibodies. Autoantibodies against N-methyl-D-aspartate, γ-aminobutyric acid A, and other known receptors and cell surface proteins were all negative (methods in appendix e-1, links.lww.com/NXI/A141). The indicated patient's antibodies were absent in samples of CSF obtained during HSE (data not shown). With the diagnosis of AE post-HSE, she was started on high-dose IV steroids and immunoglobulins without a clear improvement. Subsequently, rituximab (2 doses 500 mg/m2 2 weeks apart) resulted in neurologic improvement. A CSF sample obtained 4 months later was no longer reactive with brain. Discussion We report a young girl with recurrent HSE and a new TLR3 mutation associated with absent interferon-β responses to TLR3 agonist who several months after the first HSE episode developed recurrent HSE followed by AE. TLR3-pathway deficient patients, especially TLR3-deficient, are prone to develop HSE relapses, putting them at risk of developing AE. Indeed, a recent series of patients with HSE showed that 27% subsequently developed AE; none of them were investigated for TLR3-pathway deficiency but the current case indicates that patients with this deficiency are also at risk of AE. The symptoms of our patient (predominant behavioral abnormalities) are typical of AE post-HSE in patients older than 4 years3,4; yet the long interval between HSE and AE (17 months since the onset of HSE and 12 months since the relapse of HSE) is somewhat atypical (median 26 days in children aged 4 years or younger and 43 days in patients older than 4 years),3,5 but similar prolonged intervals occurred in 7% of patients in a recently reported series.3 The exact mechanisms underlying this severe immune-mediated complication are unknown. It has been postulated that the neuronal destruction caused by the virus leads to a release of antigens, which in the context of severe inflammation results in neuronal autoimmunity, such as that shown in our patient.3 In patients with TLR3-pathway deficiency, the increased number of episodes of HSE theoretically increases the risk of this autoimmune complication. Our case suggests that patients with recurrent HSE or family history of HSE or HSV keratitis should be assessed for TLR3-pathway deficiency.1,6,7 If the function of this pathway is impaired, patients should be carefully followed for potential relapses of HSE or AE post-HSE. Study funding This study was supported in part by Mutua Madrileña Foundation Award (AP162572016, T.A.); Plan Nacional de I+D+i and cofinanced by the ISCIII—Subdirección General de Evaluación y Formento de la Investigación Sanitaria—and the Fondo Europeo de Desarrollo Regional (ISCIII-FEDER; PI18-00486 to T.A.; 17/00234 to J.D., PI15/01094, PFIS0200 (AC16/00025), and PI18/00223 to L.A.; PI14/00616 and PI17/00543 to R.P.d.D.); Pla estratègic de recerca i innovació en salut (PERIS), Departament de Salut, Generalitat de Catalunya (SLT006/17/00362 to T.A.; SLT006/17/00199 to L.A.); a 2017 Leonardo Grant for Researchers and Cultural Creators, BBVA Foundation to L.A.; Ramon Areces Foundation, through a grant from the XVII Concurso Nacional de Ayudas a la Investigación to L.A.; and Fundació CELLEX to J.D. Disclosure J. Dalmau holds patents for the use of Ma2, NMDAR, GABAbR, GABAaR, DPPX, and IgLON5 as autoantibody tests and receives royalties related to autoantibody tests from Athena Diagnostics and Euroimmun, Inc., and is editor of Neurology®: Neuroimmunology & Neuroinflammation. The other authors declare no conflict of interest related to this manuscript. Go to Neurology.org/NN for full disclosures. Acknowledgment The authors thank Maria Rodés, Marta Muñoz, Mercè Alba, Eva Caballero, and Esther Aguilar for excellent administrative and technical support. Appendix Authors Footnotes Go to Neurology.org/NN for full disclosures. Funding information is provided at the end of the article. ↵* Shared first authorship. The Article Processing Charge was funded by Mutua Madrileña Foundation. Received June 21, 2019. Accepted in final form July 26, 2019. Copyright © 2019 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.↵Lim HK, Seppänen M, Hautala T, et al. TLR3 deficiency in herpes simplex encephalitis: high allelic heterogeneity and recurrence risk. Neurology 2014;83:1888–1897.OpenUrlCrossRefPubMed 2.↵Lafaille FG, Pessach IM, Zhang SY, et al. Impaired intrinsic immunity to HSV-1 in human iPSC-derived TLR3-deficient CNS cells. Nature 2012;491:769–773.OpenUrlCrossRefPubMed 3.↵Armangue T, Spatola M, Vlagea A, et al. Frequency, syndromes, risk factors, and outcome of autoimmune encephalitis following herpes simplex encephalitis: a prospective observational study and a retrospective analysis of cases. Lancet Neurol 2018;17:760–772.OpenUrl 4.↵Armangue T, Moris G, Cantarín-Extremera V, et al. Autoimmune post–herpes simplex encephalitis of adults and teenagers. Neurology 2015;85:1736–1743.OpenUrlPubMed 5.↵Nosadini M, Mohammad S, Corazza F, et al. Herpes simplex virus-induced anti-N-methyl-d-aspartate receptor encephalitis: a systematic literature review with analysis of 43 cases. Dev Med Child Neurol 2017;59:796–805.OpenUrl 6.↵Routes J, Abinun M, Al-Herz W, et al. ICON: the early diagnosis of congenital immunodeficiencies. J Clin Immunol 2014;34:398–424.OpenUrlPubMed 7.↵Abel L, Plancoulaine S, Jouanguy E, et al. Age-dependent Mendelian predisposition to herpes simplex virus type 1 encephalitis in childhood. J Pediatr 2010;157:623–629, 629.e1.OpenUrlCrossRefPubMed
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Frontiers | Innate Immunity in the Central Nervous System: A Missing Piece of the Autoimmune Encephalitis Puzzle? | Immunology

Frontiers | Innate Immunity in the Central Nervous System: A Missing Piece of the Autoimmune Encephalitis Puzzle? | Immunology | AntiNMDA | Scoop.it
The autoimmune encephalitides are a group of autoimmune conditions targeting the central nervous system and causing severe clinical symptoms including drug-resistant seizures, cognitive dysfunction and psychiatric disturbance.
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Gait Disturbance as the Presenting Symptom in Young Children With Anti-NMDA Receptor Encephalitis. - PubMed - NCBI

Gait Disturbance as the Presenting Symptom in Young Children With Anti-NMDA Receptor Encephalitis. - PubMed - NCBI | AntiNMDA | Scoop.it
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
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Clinical, radiological and laboratory comparison between autoantibody-negative and autoantibody-positive Autoimmune Encephalitis patients. (P2.2-006) | Neurology

Clinical, radiological and laboratory comparison between autoantibody-negative and autoantibody-positive Autoimmune Encephalitis patients. (P2.2-006) | Neurology | AntiNMDA | Scoop.it
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Anti-N-Methyl d-Aspartate Receptor Encephalitis and Electroconvulsive Therapy: Literature Review and Future Directions. - PubMed - NCBI

Anti-N-Methyl d-Aspartate Receptor Encephalitis and Electroconvulsive Therapy: Literature Review and Future Directions. - PubMed - NCBI | AntiNMDA | Scoop.it
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
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What are the HLA risk factors for NMDAR autoimmune encephalitis? –

What are the HLA risk factors for NMDAR autoimmune encephalitis? – | AntiNMDA | Scoop.it
HLA class II allele DRB1*16:02is associated with anti-NMDAR encephalitis. Shu Y, Qiu W, Zheng J, et al. JNNP 2019; 90:652-658. Abstract BACKGROUND: Aetiology and pathogenesis of anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis, the most common autoimmune encephalitis, is largely unknown.
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Winning Entry for The Anti-NMDA Receptor Encephalitis Foundation’s Prize at the 54th Congress of the Canadian Neurological Sciences Federation (CNSF)

Winning Entry for The Anti-NMDA Receptor Encephalitis Foundation’s Prize at the 54th Congress of the Canadian Neurological Sciences Federation (CNSF) | AntiNMDA | Scoop.it
The Foundation was pleased to sponsor two prizes for the best abstracts in Autoimmune Encephalitis at the recent Conference of the CNSF in Montreal, June ...Read More...
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Relapse risk factors in anti‐N‐methyl‐D‐aspartate receptor encephalitis - Nosadini - 2019 - Developmental Medicine & Child Neurology - Wiley Online Library

Relapse risk factors in anti‐N‐methyl‐D‐aspartate receptor encephalitis - Nosadini - 2019 - Developmental Medicine & Child Neurology - Wiley Online Library | AntiNMDA | Scoop.it
Aim To identify factors that may predict and affect the risk of relapse in anti‐N‐methyl‐D‐aspartate receptor (NMDAR) encephalitis. Method This was a retrospective study of an Italian cohort of pat...
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Cerebrospinal Fluid Findings in Patients With Autoimmune Encephalitis-A Systematic Analysis | Read by QxMD

Cerebrospinal Fluid Findings in Patients With Autoimmune Encephalitis-A Systematic Analysis | Read by QxMD | AntiNMDA | Scoop.it
Cerebrospinal Fluid Findings in Patients With Autoimmune Encephalitis-A Systematic Analysis Tetyana Blinder, Jan Lewerenz Frontiers in Neurology 2019, 10: 804 Autoimmune encephalitides (AIE) comprise a group of inflammatory diseases of the central nervous system (CNS), which can be further characterized by the presence of different antineuronal antibodies. Recently, a clinical approach for diagnostic criteria for the suspected diagnosis of AIE as well as definitive AIE were proposed. These are intended to guide physicians when to order the antineuronal antibody testing and/or facilitate early diagnosis even prior to the availability of the specific disease-confirming test results to facilitate prompt treatment. These diagnostic criteria also include the results of basic cerebrospinal fluid (CSF) analysis. However, the different antibody-defined AIE subtypes might be highly distinct with regard to their immune pathophysiology, e.g., the pre-dominance of specific IgG subclasses, IgG1, or IgG4, or frequency of paraneoplastic compared to idiopathic origin. Thus, it is conceivable that the results of basic CSF analysis might also be very different. However, this has not been explored systematically. Here, we systematically reviewed the literature about the 10 most important AIE subtypes, AIE with antibodies against NMDA, AMPA, glycine, GABAA , and GABAB receptors as well as DPPX, CASPR2, LGI1, IgLON5, or glutamate decarboxylase (GAD), with respect to the reported basic CSF findings comprising CSF leukocyte count, total protein, and the presence of oligoclonal bands (OCB) restricted to the CSF as a sensitive measure for intrathecal IgG synthesis. Our results indicate that these basic CSF findings are profoundly different among the 10 different AIE subtypes. Whereas, AIEs with antibodies against NMDA, GABAB , and AMPA receptors as well as DPPX show rather frequent inflammatory CSF changes, in AIEs with either CASPR2, LGI1, GABAA , or glycine receptor antibodies CSF findings were mostly normal. Two subtypes, AIEs defined by either GAD, or IgLON5 antibodies, did not fit into this general pattern. In AIE with GAD antibodies, positive OCBs in the absence of other changes were typical, while the CSF in IgLON5 antibody-positive AIE was characterized by elevated protein. Comments You need to log in or sign up for an account to be able to comment. No comments yet, be the first to post one! Related Papers
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West Nile Virus infection triggering autoimmune encephalitis: Pathophysiological and therapeutic implications. - PubMed - NCBI

West Nile Virus infection triggering autoimmune encephalitis: Pathophysiological and therapeutic implications. - PubMed - NCBI | AntiNMDA | Scoop.it
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
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