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Clinical significance of anti-NMDAR concurrent with glial or neuronal surface antibodies. - PubMed - NCBI

Clinical significance of anti-NMDAR concurrent with glial or neuronal surface antibodies. - 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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Covid-19 and encephalitis - podcast

Covid-19 and encephalitis - podcast | AntiNMDA | Scoop.it
A podcast answering your questions about Covid-19 (Coronavirus) and encephalitis. Filmed on March 20.
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Little girl’s angry outbursts which were put down to sinusitis turned out to be brain condition - Cambridgeshire Live

Little girl’s angry outbursts which were put down to sinusitis turned out to be brain condition - Cambridgeshire Live | AntiNMDA | Scoop.it
Doctors initially thought six-year-old Amelia’s unfamiliar behaviour was down to sinus problems, before diagnosing an incurable brain condition...
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Screening for anti-NMDAR Encephalitis in Psychiatry

Anti-NMDAR encephalitis most commonly presents to psychiatric services, so early identification of this disorder is essential. We aim to validate the two screening criteria (Scott et al.and Herken and Pruss) which have been proposed to identify first episode psychosis patients who should have anti-...
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Case Report: Autoimmune Encephalitis in Patient With Crohn Disease and Ankylosing Spondylitis Receiving Infliximab

Case Report: Autoimmune Encephalitis in Patient With Crohn Disease and Ankylosing Spondylitis Receiving Infliximab | AntiNMDA | Scoop.it
In this case study presented at ACTRIMS 2020, researchers reported on data from a patient with Crohn disease and ankylosing spondylitis who developed autoimmune encephalitis while receiving infliximab.
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The Strange Link Between Pandemics and Psychosis - VICE

The Strange Link Between Pandemics and Psychosis - VICE | AntiNMDA | Scoop.it
Scientists are looking more closely at how viruses and infections could influence our minds.
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Autoimmune encephalitis in children: clinical phenomenology, therapeutics, and emerging challenges. - PubMed - NCBI

Autoimmune encephalitis in children: clinical phenomenology, therapeutics, and emerging challenges. - 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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My near-death experience with encephalitis

My near-death experience with encephalitis | AntiNMDA | Scoop.it
My name is Kertisha Brabson. I was left fighting for my life when I developed a rare autoimmune disease that can attack the brain. This is my story.
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The autoantibody-mediated encephalitides: from clinical observations to molecular pathogenesis | SpringerLink

The autoantibody-mediated encephalitides: from clinical observations to molecular pathogenesis | SpringerLink | AntiNMDA | Scoop.it
The autoimmune encephalitis (AE) syndromes have been characterised by the detection of autoantibodies in serum and/or cerebrospinal fluid which target the extracellular domains of specific neuroglial antigens.
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Autoimmune Encephalitis in Children

Autoimmune Encephalitis in Children | AntiNMDA | Scoop.it
The causes of encephalitis are numerous, and extensive investigations for infectious agents and other etiologies are often negative. The discovery that many of these encephalitis are immune mediated has changed the approach to the diagnosis and treatment ...
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Plasma exchange in neurological disease | Practical Neurology

Plasma exchange in neurological disease | Practical Neurology | AntiNMDA | Scoop.it
Review Plasma exchange in neurological disease Chinar Osman1, Rachel Jennings1, Khaled El-Ghariani2, Ashwin Pinto1 Neurosciences, Wessex Neurological Centre, Southampton, UK Therapeutics and Tissue Services, NHS Blood and Transplant, Sheffield Teaching Hospitals NHS Trust and the University of Sheffield, Sheffield, UK Correspondence to Dr Chinar Osman, Neurosciences, Wessex Neurological Centre, Southampton SO16 6YD, UK; chinar.osman{at}uhs.nhs.uk Abstract Plasma exchange is a highly efficient technique to remove circulating autoantibodies and other humoral factors rapidly from the vascular compartment. It was the first effective acute treatment for peripheral disorders such as Guillain-Barré syndrome and myasthenia gravis before intravenous immunoglobulin became available. The recent recognition of rapidly progressive severe antibody-mediated central nervous system disorders, such as neuromyelitis optica spectrum disorders and anti-N-methyl-D-aspartate-receptor encephalitis, has renewed interest in using plasma exchange for their acute treatment also. In this review we explain the principles and technical aspects of plasma exchange, review its current indications, and discuss the implications for its provision in the UK. View Full Text Statistics from Altmetric.com View Full Text Footnotes Contributors CO wrote the draft manuscript. RJ and KE-G contributed to the practicalities of PLEX. AAP reviewed the manuscript. 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 None declared. Patient consent for publication Not required. Provenance and peer review Commissioned. Externally peer reviewed by Marguerite Hill, Swansea, UK and Aisling Carr, London, UK 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)) 2020. 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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Angie’s Story, Age 39 years, Ohio, U.S.A.

Angie’s Story, Age 39 years, Ohio, U.S.A. | AntiNMDA | Scoop.it
Angie was a busy, young working-from-home wife and mother until July 2019 when Anti-NMDA Receptor Encephalitis turned her and her family’s life upside down. Here ...Read More...
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Clinical significance of anti-NMDAR concurrent with glial or neuronal surface antibodies | Neurology

Clinical significance of anti-NMDAR concurrent with glial or neuronal surface antibodies | Neurology | AntiNMDA | Scoop.it
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Elsevier offers free content for Rare Disease Day

Starting February 29, 2020, Elsevier will make clinical review articles and book chapters openly accessible for 60 days to raise awareness of rare diseases...
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Neuropsychological and psychiatric outcomes in encephalitis: A multi-centre case-control study

Neuropsychological and psychiatric outcomes in encephalitis: A multi-centre case-control study | AntiNMDA | Scoop.it
Objectives Our aim was to compare neuropsychological and psychiatric outcomes across three encephalitis aetiological groups: Herpes simplex virus (HSV), other infections or autoimmune causes (Other), and encephalitis of unknown cause (Unknown). Methods Patients recruited from NHS hospitals underwent neuropsychological and psychiatric assessment in the short-term (4 months post-discharge), medium-term (9–12 months after the first assessment), and long-term (>1-year). Healthy control subjects were recruited from the general population and completed the same assessments. Results Patients with HSV were most severely impaired on anterograde and retrograde memory tasks. In the short-term, they also showed executive, IQ, and naming deficits, which resolved in the long-term. Patients with Other or Unknown causes of encephalitis showed moderate memory impairments, but no significant impairment on executive tests. Memory impairment was associated with hippocampal/medial temporal damage on magnetic resonance imaging (MRI), and naming impairment with left temporal and left frontal abnormalities. Patients reported more subjective cognitive complaints than healthy controls, with tiredness a significant problem, and there were high rates of depression and anxiety in the HSV and the Other encephalitis groups. These subjective, self-reported complaints, depression, and anxiety persisted even after objectively measured neuropsychological performance had improved. Conclusions Neuropsychological and psychiatric outcomes after encephalitis vary according to aetiology. Memory and naming are severely affected in HSV, and less so in other forms. Neuropsychological functioning improves over time, particularly in those with more severe short-term impairments, but subjective cognitive complaints, depression, and anxiety persist, and should be addressed in rehabilitation programmes.
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Anti-Hu limbic encephalitis preceding the appearance of mediastinal germinoma by 9 years | Neurology Neuroimmunology & Neuroinflammation

Anti-Hu limbic encephalitis preceding the appearance of mediastinal germinoma by 9 years | Neurology Neuroimmunology & Neuroinflammation | AntiNMDA | Scoop.it
Autoimmune limbic encephalitis is characterized by the subacute onset of seizures, short-term memory loss, and confusion and can have a paraneoplastic or nonparaneoplastic etiology.1 Anti-Hu limbic encephalitis is typically paraneoplastic, most frequently associated with small-cell lung cancer.2 We report the case of a 28-year-old man diagnosed with a mediastinal germ cell tumor 9 years after presenting with anti-Hu-positive limbic encephalitis. Case report A 19-year-old man presented after a generalized tonic-clonic seizure after several days of headaches and confusion. He had no medical history and did not take regular medications. There was no history of drug use, and he was a nonsmoker. There was no focal neurologic deficit on examination. Electroencephalography demonstrated right temporal spike and slow wave activity. Brain MRI showed hyperintensity in the right medial temporal lobe on T2 FLAIR sequence, without gadolinium enhancement (figure, A). CSF showed 3 monocytes, and the protein level was slightly elevated (0.48 g/L, NR 0.15–0.45 g/L). He was diagnosed with viral encephalitis. Figure Imaging investigations (A) Axial T2 fluid attenuated inversion recovery (FLAIR) MRI of the brain showing hyperintensity in the right medial temporal lobe at the age of 22 years. (B) Large anterior mediastinal mass diagnosed at the age of 28 years as demonstrated on CT chest. (C) Large anterior mediastinal mass (age 28) demonstrating high glucose avidity on PET-CT. (D) Left: Markedly increased metabolism in the left anteromesial temporal lobe and hippocampus. Right: Resolution of those changes 11 months after resection of the mediastinal tumor. At the age of 21 years, he re-presented with seizures, confusion, emotional lability, night sweats, and short-term memory loss. MRI demonstrated ongoing T2 FLAIR hyperintensity in the right medial temporal lobe. Further workup revealed serum anti-Hu antibodies by immunofluorescence (Inova Diagnostics, CA), confirmed by line immunoblot (Euroimmun Lubeck, Germany). Other antibodies, including amphiphysin, CRMP5, Ma2, Yo, Ri, titin, recoverin, SOX-1, and VGKC, were negative. He was diagnosed with paraneoplastic limbic encephalitis as per the guidelines by Graus.1 The CT scan of chest, abdomen, and pelvis was negative for malignancy, and whole-body PET was normal. Ultrasound revealed microcalcifications in the right testis. Alfa-fetoprotein and β-human chorionic gonadotropin (β-hCG) were negative. He was managed with IV cyclophosphamide 0.75 g/m2 monthly for 6 months as per the National Institute of Health (NIH) protocol, IV methylprednisolone 1000 mg daily for 5 days, and IV immunoglobulin (IVIG) 0.4 g/kg/d for 5 days. This was followed by oral prednisone 50 mg daily, weaned to 10 mg daily after several weeks, azathioprine 50 mg twice daily (1.33 mg/kg/d), IVIG 0.4 g/kg 1 day per month, and antiepileptic therapy. His condition followed a fluctuating course, and repeated malignancy screening remained negative. Right orchiectomy was performed at the age of 24 years; however, findings were nonspecific and his condition remained unchanged. At the age of 26 years, a single course of rituximab 1000 mg was given in response to radiologic relapse, after which neuropsychometric parameters and MRI mildly improved. Azathioprine and IVIG continued throughout; prednisone was ceased after a slow wean over 3 years. At the age of 28 years, he re-presented with pleuritic chest pain. CT scan demonstrated a large anterior mediastinal soft-tissue lesion measuring 107 mm, which was highly glucose avid on PET (figure, B and C). Biopsy revealed a nonseminomatous germ cell tumor. Serum alfa-fetoprotein was 954 kIU/L (NR 0–6), and serum β-hCG 19 IU/L (NR 0–5). Serum anti-Hu remained positive, and all other antibodies remained negative. Immunotherapy was ceased, and he received bleomycin, etoposide, and cisplatin (BEP) 2 months before surgical resection. Pathologic assessment showed a mixed germ cell tumor with low grade sarcomatous components. Immunohistochemistry was performed on permeabilized formalin-fixed paraffin-embedded tissue with HuD antibody at a dilution of 1:100 on an automated Leica Bond III. Tumor tissue was compared with normal brain as a positive control; however, it did not stain positive. He has been neurologically stable for 3 years postoperatively and has now been able to undertake a vocational training course. He is no longer receiving immunotherapy. Lung recurrences 6 months and 2 years postoperatively required repeat resection and chemoradiotherapy. Neurologic PET, 11 months postoperatively, demonstrated resolution of previously persistent temporal lobe changes (figure, D). Discussion Our patient presented with paraneoplastic limbic encephalitis, presumably since the age of 19 years. However, it was not until 9 years later that malignancy was detected. Paraneoplastic limbic encephalitis frequently precedes the diagnosis of an underlying malignancy;2 however, the current criteria for diagnosis include demonstration of malignancy within 42 or 51 years. Anti-Hu antibodies are associated with malignancy in more than 95% of cases, so the eventual detection of malignancy as in our case should not be surprising. It is more typical that Hu antibodies are associated with small-cell lung cancer,3 although a mediastinal germinoma has been reported.4 It is possible that testicular microcalcifications were evidence of earlier immunologic activity, especially given the development of a germ cell tumor. This very long delay between Hu antibody positivity and the diagnosis of malignancy is atypical. Similar cases include detection of small-cell lung cancer 5.5 years after anti-Hu-associated subacute sensory neuronopathy,5 lung carcinoid detected 8 years after initial diagnosis of anti-Ri antibodies,6 and 2 patients in whom malignancy developed 4.5 and 10 years, respectively, after detection of anti-Yo antibody-associated cerebellar degeneration.7 Although our patient's tumor did not stain positive for anti-Hu, it was likely responsible for his syndrome, as evidenced by his improvement after resection. Negative staining might be explained by preanalytical fixation of the tissue influencing the binding capacity of the antibody or a lack of specificity to particular epitopes on the tumor itself. The long delay between the detection of anti-Hu antibodies and the diagnosis of malignancy in this case highlights the importance of ongoing surveillance for malignancy in the presence of onconeuronal antibodies. Study Funding No targeted funding reported. Disclosure The authors report no disclosures. Go to Neurology.org/NN for full disclosures. Appendix Authors Footnotes Go to Neurology.org/NN for full disclosures. Funding information is provided at the end of the article. The Article Processing Charge was funded by Concord Repatriation General Hospital. Received November 5, 2019. Accepted in final form January 23, 2020. 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.↵Graus F, Delattre JY, Antoine JC, et al. Recommended diagnostic criteria for paraneoplastic neurological syndromes. J Neurol Neurosurg Psychiatr 2004;75:1135–1140. 2.↵Gultekin SH, Rosenfeld MR, Voltz R, Eichen J, Posner JB, Dalmau J. Paraneoplastic limbic encephalitis: neurological symptoms, immunological findings and tumour association in 50 patients. Brain 2000;123:1481–1494.OpenUrlCrossRefPubMed 3.↵Graus F, Titulaer MJ, Balu R, et al. A clinical approach to diagnosis of autoimmune encephalitis. Lancet Neurol 2016;15:391–404.OpenUrlCrossRefPubMed 4.↵Nanavati A, Zeck J, Philips G, Bade NA. A unique case of pronounced neurologic deficit from paraneoplastic syndrome that precedes appearance of mediastinal germinoma by two years. Case Rep Clin Pathol 2016;3:6–9.OpenUrl 5.↵Gaillard N, Charif M, Carlander B, Pujol JL, Touchon J. Chemotherapy treatment for anti-Hu paraneoplastic syndrome without active malignancy [in French]. Rev Neurol (Paris) 2006;162:862–865.OpenUrlPubMed 6.↵Harloff A, Hummel S, Kleinschmidt M, Rauer S. Anti-Ri antibodies and limbic encephalitis in a patient with carcinoid tumour of the lung. J Neurol 2005;252:1404–1405.OpenUrlCrossRefPubMed 7.↵Rojas-Marcos I, Rousseau A, Keime-Guibert F, et al. Spectrum of paraneoplastic neurologic disorders in women with breast and gynecologic cancer. Medicine (Baltimore) 2003;82:216–223.OpenUrlCrossRefPubMed
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Anti-N-methyl-d-aspartate receptor encephalitis: A primer for acute care healthcare professionals - Dustin Anderson, Nabeela Nathoo, Jennifer A McCombe, Penelope Smyth, Peter G Brindley,

Anti-N-methyl-d-aspartate receptor encephalitis: A primer for acute care healthcare professionals - Dustin Anderson, Nabeela Nathoo, Jennifer A McCombe, Penelope Smyth, Peter G Brindley, | AntiNMDA | Scoop.it
This primer summarizes the diagnosis, treatment, complications, and prognosis of anti-N-methyl-d-aspartate receptor encephalitis for healthcare professionals, especially those in acute care special...
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GOOD NEWS – Congratulations Dr. Budhram!

GOOD NEWS – Congratulations Dr. Budhram! | AntiNMDA | Scoop.it
In these worrying times of the novel corona virus or covid19 as it is officially known, we are pleased to share some good news with ...Read More...
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Clinical significance of anti-NMDAR concurrent with glial or neuronal surface antibodies. - PubMed - NCBI

Clinical significance of anti-NMDAR concurrent with glial or neuronal surface antibodies. - 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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A rare disease and an uncommon resilience

A rare disease and an uncommon resilience | AntiNMDA | Scoop.it
She was a patient without a diagnosis. From the spring of 2016 to that winter, Emily Chan bounced from the neurology department to the psychiatric department and back again as health-care . . .
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Aroon: Healing with Art | UCSF Benioff Children's Hospitals

Aroon: Healing with Art | UCSF Benioff Children's Hospitals | AntiNMDA | Scoop.it
Athletic, coordinated, confident. That’s how Joy would describe her 5-year-old son Aroon, who loved to emulate ninjas with feisty kicks and had been scouted as a model. But suddenly Aroon was tripping down stairs and wobbling like a newborn fawn when he walked. Aroon’s primary doctor near their Stockton home said the kindergartner seemed fine. “But my mommy instinct knew he wasn’t,” Joy says. Test after test failed to explain Aroon’s confusing symptoms, which gradually became more acute. Aroon began to erupt in violent tantrums: flailing wildly, pulling his hair, holding his breath until he turned blue. “Mom, I’m so sorry,” Joy recalls Aroon explaining. “There is something inside of me that I can’t control.” That’s when Joy brought Aroon to UCSF Benioff Children's Hospital Oakland. He was diagnosed with anti-NMDA receptor encephalitis, a rare disease that causes the immune system to attack parts of the brain that control judgment, perception of reality, memory, and basic functions like breathing and swallowing. During the nearly one year Aroon spent in the hospital, his condition deteriorated to the point that he became unable to move and could communicate only by blinking. With each victory seemed to come a setback. Aroon would regain some abilities only to lose them again, slipping further away. One constant in Aroon’s life was art. At UCSF Benioff Oakland, child life specialists and artists-in-residence work with patients to support their healing through creative expression. “That team played such an important role in his recovery,” Joy says. “Consistently doing art was crucial. No matter how severe Aroon’s condition, the staff got creative and found a way to make art with him.” An adaptive device that extended the length of a regular paintbrush, for example, allowed Aroon to create art with just small movements of his fingertips. Aroon’s caregivers were also a vital part of the family’s journey. Nurses blasted music and sang with Aroon, celebrated his birthday, and even took care of his younger brother so Joy could rest. “I had nights when I just cried and cried,” Joy says. “The staff was so supportive. They became like family.” Through diligent daily therapies, the compassionate care of his multidisciplinary medical team, and the unwavering support of his family, Aroon eventually became well enough to return home.
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“Brain on Fire” film helps patient receive diagnosis - News | UAB

“Brain on Fire” film helps patient receive diagnosis - News | UAB | AntiNMDA | Scoop.it
With almost $200 million in NIH funding, UAB scientists are at the forefront of research that is shaping the future of health and healthcare.
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HLA class II allele DRB1*16:02 is associated with anti-NMDAR encephalitis. - PubMed - NCBI

HLA class II allele DRB1*16:02 is associated with anti-NMDAR 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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Th17 lymphocytes drive vascular and neuronal deficits in a mouse model of postinfectious autoimmune encephalitis | PNAS

Th17 lymphocytes drive vascular and neuronal deficits in a mouse model of postinfectious autoimmune encephalitis | PNAS | AntiNMDA | Scoop.it
Significance Antibodies against neuronal receptors and synaptic proteins are associated with a group of ill-defined central nervous system (CNS) autoimmune diseases named autoimmune encephalitides (AE), characterized by an abrupt onset of seizures and movement and psychiatric deficits. How these antibodies enter the brain to trigger neuroinflammation, and how they affect the function of neural circuits, remains poorly understood. Here, we demonstrate that Th17 lymphocytes are critical for entry of autoantibodies into the CNS, persistent microglia activation, and neurophysiological deficits in odor processing, in a mouse model of postinfectious autoimmune encephalitis triggered by multiple infections with group A Streptococcus. Our findings emphasize the critical role that Th17 lymphocytes play in disease pathogenesis to impair CNS function in AE syndromes. Abstract Antibodies against neuronal receptors and synaptic proteins are associated with a group of ill-defined central nervous system (CNS) autoimmune diseases termed autoimmune encephalitides (AE), which are characterized by abrupt onset of seizures and/or movement and psychiatric symptoms. Basal ganglia encephalitis (BGE), representing a subset of AE syndromes, is triggered in children by repeated group A Streptococcus (GAS) infections that lead to neuropsychiatric symptoms. We have previously shown that multiple GAS infections of mice induce migration of Th17 lymphocytes from the nose into the brain, causing blood–brain barrier (BBB) breakdown, extravasation of autoantibodies into the CNS, and loss of excitatory synapses within the olfactory bulb (OB). Whether these pathologies induce functional olfactory deficits, and the mechanistic role of Th17 lymphocytes, is unknown. Here, we demonstrate that, whereas loss of excitatory synapses in the OB is transient after multiple GAS infections, functional deficits in odor processing persist. Moreover, mice lacking Th17 lymphocytes have reduced BBB leakage, microglial activation, and antibody infiltration into the CNS, and have their olfactory function partially restored. Th17 lymphocytes are therefore critical for selective CNS entry of autoantibodies, microglial activation, and neural circuit impairment during postinfectious BGE. Footnotes ↵1To whom correspondence may be addressed. Email: franks{at}neuro.duke.edu or da191{at}cumc.columbia.edu. Author contributions: M.P.P., T.C., K.M.F., and D.A. designed research; M.P.P., K.A.B., C.R.W., S.C., T.C., K.M.F., and D.A. performed research; K.A.B. contributed new reagents/analytic tools; M.P.P., K.A.B., C.R.W., S.C., T.C., K.M.F., and D.A. analyzed data; and M.P.P., K.A.B., C.R.W., T.C., K.M.F., and D.A. 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.1911097117/-/DCSupplemental. Published under the PNAS license.
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Clinical features of seronegative, but CSF antibody-positive, anti-NMDA receptor encephalitis | Neurology Neuroimmunology & Neuroinflammation

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