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Increased rates of sequelae post-encephalitis in individuals attending primary care practices in the United Kingdom: a population-based retrospective cohort study

Increased rates of sequelae post-encephalitis in individuals attending primary care practices in the United Kingdom: a population-based retrospective cohort study | AntiNMDA | Scoop.it
Journal of Neurology February 2017, Volume 264, Issue 2, pp 407–415 | Cite as Increased rates of sequelae post-encephalitis in individuals attending primary care practices in the United Kingdom: a population-based retrospective cohort study Authors Authors and affiliations Julia GranerodEmail author Nicholas W. S. Davies Parashar P. Ramanuj Ava Easton David W. G. Brown Sara L. Thomas Neurological Update First Online: 20 October 2016 Received: 06 October 2016 Revised: 12 October 2016 Accepted: 12 October 2016 34 Shares 192 Downloads 1 Citations Abstract The true extent of sequelae in encephalitis survivors relative to rates within the general population is not known. This study aimed to quantify increased risks of epilepsy, depressive disorders, anxiety disorders, psychotic disorders, bipolar disorder, cognitive problems, dementia, headache, and alcohol abuse among encephalitis cases. 2460 exposed individuals diagnosed with incident encephalitis in the Clinical Practice Research Datalink and 47,914 unexposed individuals without a history of encephalitis were included. Multivariable Poisson regression was used to estimate adjusted rate ratios in individuals with encephalitis compared to the general population and to estimate whether the effect of these outcomes varied over time. Individuals with encephalitis had an increased risk of all investigated outcomes. The highest RR was seen for epilepsy (adjusted RR 31.9; 95 % confidence interval 25.38–40.08), whereas the lowest was seen for anxiety disorders (1.46, 1.27–1.68). The second highest RRs were for particular psychiatric illnesses, including bipolar disorder (6.34, 3.34–12.04) and psychotic disorders (3.48, 2.18–5.57). The RR was highest in the first year of follow-up for all outcomes except headache; this was particularly true for epilepsy (adjusted RR in first year of follow-up 139.6, 90.62–215.03). This study shows that sequelae are common in survivors of encephalitis. We confirm the presence of outcomes more commonly linked to encephalitis and describe those less commonly identified as being associated with encephalitis. The results of this study have important implications for the management of encephalitis patients and for the design of tertiary prevention strategies, as many of these sequelae are treatable. Keywords Epidemiology Outcomes Encephalitis Epilepsy Sequelae  This is a preview of subscription content, log in to check access Notes Acknowledgments The authors thank Harriet Forbes for extraction of the data. Compliance with ethical standards Funding This report is independent research commissioned and funded by the Department of Health’s Policy Research Programme (Enhanced Diagnostic and Management Strategies to Improve the Identification and Outcome of Individuals with Encephalitis, 047/1084). The views expressed in this publication are those of the author(s) and not necessarily those of the Department of Health. Ethics This study was approved by the Independent Scientific Advisory Committee of the Medicines and Healthcare Products Regulatory Authority (ISAC_09_061RA2) and the Ethics Committee of the London School of Hygiene and Tropical Medicine. Conflicts of interest The authors declare that they have no conflict of interest. Data sharing No additional data available. Supplementary material 415_2016_8316_MOESM1_ESM.docx (22 kb) Supplementary material 1 (DOCX 21 kb) References 1. Granerod J, Tam CC, Crowcroft NS, Davies NWS, Borchert M, Thomas SL (2010) Challenge of the unknown: a systematic review of acute encephalitis in non-outbreak situations. Neurology 75(10):924–932 CrossRefPubMedGoogle Scholar 2. Irani SR, Alexander S, Waters P et al (2010) Antibodies to Kv1 potassium channel-complex proteins leucine-rich, glioma inactivated 1 protein and contactin-associated protein-2 in limbic encephalitis, Morvan’s syndrome and acquired neuromyotonia. Brain 133(9):2734–2748 CrossRefPubMedPubMedCentralGoogle Scholar 3. Dalmau J, Lancaster E, Martinez-Hernandez E, Rosenfeld MR, Balice-Gordon R (2011) Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis. Lancet Neurol 10(1):63–74 CrossRefPubMedPubMedCentralGoogle Scholar 4. Granerod J, Cousens S, Davies NWS, Crowcroft NS, Thomas SL (2013) New estimates of incidence of encephalitis in England. Emerg Infect Dis. doi: 10.3201/eid1909.130064 PubMedPubMedCentralGoogle Scholar 5. Easton A, Atkin K, Dowell E (2006) Encephalitis, a service orphan: the need for more research and access to neuropsychology. Br J Neurosci Nurs 2:488–492 CrossRefGoogle Scholar 6. Granerod J, Ambrose HE, Davies NW et al (2010) Causes of encephalitis and differences in their clinical presentations in England: a multicentre, population-based prospective study. Lancet Infect Dis 10(12):835–844 CrossRefPubMedGoogle Scholar 7. Easton A (2016) Life after encephalitis: a narrative approach. Routledge, Oxford Google Scholar 8. Hjalmarsson A, Blomqvist P, Skoldenberg B (2007) Herpes simplex encephalitis in Sweden, 1990–2001: incidence, morbidity, and mortality. Clin Infect Dis 45:875–880 CrossRefPubMedGoogle Scholar 9. Fazekas C, Enzinger C, Wallner M et al (2006) Depressive symptoms following herpes simplex encephalitis–an underestimated phenomenon? Gen Hosp Psychiatry 28:403–407 CrossRefPubMedGoogle Scholar 10. Mailles A, De Broucker T, Costanzo P, Martinez-Almoyna L, Vaillant V, Stahl JP, Steering Committee and Investigators Group (2012) Long-term outcome of patients presenting with acute infectious encephalitis of various causes in France. Clin Infect Dis 54(10):1455–1464 CrossRefPubMedGoogle Scholar 11. Herrett E, Gallagher AM, Bhaskaran K, Forbes H, Mathur R, van Staa T et al (2015) Data Resource Profile: Clinical Practice Research Datalink (CPRD). Int J Epidemiol. doi: 10.1093/ije/dyv098 PubMedPubMedCentralGoogle Scholar 12. CPRD website. https://www.cprd.com/intro.asp 13. Herrett E, Thomas SL, Schoonen WM et al (2010) Validation and validity of diagnoses in the General Practice Research Database: a systematic review. Br J Clin Pharmacol 69:4–14 CrossRefPubMedPubMedCentralGoogle Scholar 14. Lewis JD, Bilker WB, Weinstein RB, Strom BL (2005) The relationship between time since registration and measured incidence rates in the General Practice Research Database. Pharmacoepidemiol Drug Saf 14(7):443–451. doi: 10.1002/pds.1115 CrossRefPubMedGoogle Scholar 15. Baumeister H (2012) Inappropriate prescriptions of antidepressant drugs in patients with subthreshold to mild depression: time for the evidence to become practice. J Affect Dis 139:240–243 CrossRefPubMedGoogle Scholar 16. CG90 (2009) Depression in adults: recognition and management. National Institute for Health and Care Excellence Google Scholar 17. Pillai SC, Mohammad SS, Hacohen Y, Tantsis E, Prelog K, Barnes EH, Gill D, Lim MJ, Brilot F, Vincent A, Dale RC (2016) Postencephalitic epilepsy and drug-resistant epilepsy after infectious and antibody-associated encephalitis in childhood: clinical and etiologic risk factors. Epilepsia 57(1):e7–e11 CrossRefPubMedGoogle Scholar 18. Rismanchi N, Gold JJ, Sattar S, Glaser CA, Sheriff H, Proudfoot J, Mower A, Crawford JR, Nespeca M, Wang SG (2015) Epilepsy after resolution of presumed childhood encephalitis. Pediatr Neurol 53(1):65–72 CrossRefPubMedGoogle Scholar 19. Depression after Traumatic Brain Injury was developed by J Fann and T Hart in collaboration with the Model Systems Knowledge Translation Center. http://www.msktc.org/tbi/factsheets/Depression-After-Traumatic-Brain-Injury#sthash.HlR0e0MJ.dpuf 20. Blomström Å, Karlsson H, Svensson A, Frisell T, Lee BK, Dal H, Magnusson C, Dalman C (2014) Hospital admission with infection during childhood and risk for psychotic illness—a population-based cohort study. Schizophr Bull 40(6):1518–1525 CrossRefPubMedGoogle Scholar 21. Avramopoulos D, Pearce BD, McGrath J, Wolyniec P, Wang R, Eckart N, Hatzimanolis A, Goes FS, Nestadt G, Mulle J, Coneely K, Hopkins M, Ruczinski I, Yolken R, Pulver AE (2015) Infection and inflammation in schizophrenia and bipolar disorder: a genome wide study for interactions with genetic variation. PLoS One 10(3):e0116696 CrossRefPubMedPubMedCentralGoogle Scholar 22. Hokkanen L, Launes J (1997) Cognitive recovery instead of decline after acute encephalitis: a prospective follow up study. J Neurol Neurosurg Psychiatry 63:222–227 CrossRefPubMedPubMedCentralGoogle Scholar 23. Gatson JW, Stebbins C, Mathews D, Harris TS, Madden C, Batjer H, Diaz-Arrastia R, Minei JP (2015) Evidence of increased brain amyloid in severe TBI survivors at 1, 12, and 24 months after injury: report of 2 cases. J Neurosurg 1–8 Google Scholar 24. Lucas S (2015) Posttraumatic headache: clinical characterization and management. Curr Pain Headache Rep 19(10):48 CrossRefPubMedGoogle Scholar 25. Russo A, D’Onofrio F, Conte F, Petretta V, Tedeschi G, Tessitore A (2014) Post-traumatic headaches: a clinical overview. Neurol Sci 35(1):153–156 CrossRefPubMedGoogle Scholar 26. Neligan A, Sander JW (2009) The incidence and prevalence of epilepsy. In: Sander JW, Rugg-Gunn, FJ, Smalls JE (eds) Epilepsy 2009: from benchside to bedside. A practical guide to epilepsy. Lecture notes from the Twelfth Epilepsy Teaching Weekend, 18–20 September 2009, St. Anne’s College, Oxford. International League Against Epilepsy (UK Chapter) and National Society for Epilepsy: Chalfont St Peter, Bucks, pp 15–21 Google Scholar 27. Rait G, Walters K, Griffin M, Buszewicz M, Petersen I, Nazareth I (2009) Recent trends in the incidence of recorded depression in primary care. Br J Psychiatry 195(6):520–524 CrossRefPubMedGoogle Scholar 28. Frisher M, Collins J, Millson D, Crome I, Croft P (2004) Prevalence of comorbid psychiatric illness and substance misuse in primary care in England and Wales. J Epidemiol Community Health 58(12):1036–1041 CrossRefPubMedPubMedCentralGoogle Scholar 29. Beghi E, Nicolosi A, Kurland LT et al (1984) Encephalitis and aseptic meningitis, Olmsted County, Minnesota, 1950–1981: I. Epidemiology. Ann Neurol 16:283–294 CrossRefPubMedGoogle Scholar 30. Cizman M, Jazbec J (1993) Aetiology of acute encephalitis in childhood in Slovenia. Pediatr Infect Dis J 12:903–908 CrossRefPubMedGoogle Scholar 31. Lee T, Tsai C, Yuan C, Wei C, Tsao W, Lee R, Cheih S, Huang I, Chen K (2003) Encephalitis in Taiwan: a prospective hospital-based study. Jpn J Infect Dis 56:193–199 PubMedGoogle Scholar 32. Studahl M, Bergstrom T, Hagberg L (1998) Acute viral encephalitis in adults: a prospective study. Scand J Infect Dis 30:215–220 CrossRefPubMedGoogle Scholar Copyright information © Springer-Verlag Berlin Heidelberg 2016 Authors and Affiliations Julia Granerod1Email author Nicholas W. S. Davies2 Parashar P. Ramanuj3 Ava Easton4 David W. G. Brown15 Sara L. Thomas6 1.Virus Reference DepartmentPublic Health England, National Infection ServiceLondonUK 2.Department of NeurologyChelsea and Westminster HospitalLondonUK 3.New York State Psychiatric InstituteNew YorkUSA 4.Encephalitis SocietyMaltonUK 5.Influenza LaboratoryOswaldo Cruz Institute/FiocruzRio de JaneiroBrazil 6.London School of Hygiene and Tropical MedicineLondonUK
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Neural Antibody Testing for Autoimmune Encephalitis: A Canadian Single-Centre Experience | Canadian Journal of Neurological Sciences

Neural Antibody Testing for Autoimmune Encephalitis: A Canadian Single-Centre Experience - Volume 48 Issue 6
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Autoimmune encephalitis with coexistent LGI1 and GABABR1 antibodies: case report | BMC Neurology | Full Text

Autoimmune encephalitis with coexistent LGI1 and GABABR1 antibodies: case report | BMC Neurology | Full Text | AntiNMDA | Scoop.it
Background Autoimmune encephalitis (AE) with multiple auto-antibodies is of great clinical significance because its complex clinical manifestations and atypical imaging increase the difficulty of diagnosis, differential diagnosis and treatment, which may aggravate the disease, increase the recurrence rate and mortality. The coexistence of anti-Leucinie-rich Glioma Inactivated 1 (LGI1) and anti-γ-aminobutyric acid-beta-receptor 1 (GABABR1) has not been published before. Case presentation We herein present the case of a 60-year-old man with slow response, behavioral changes, psychosis and sleep disorders. Laboratory test included serum hyponatremia, positive serum LGI1 and GABABR1 antibodies using transfected cell-based assays. Electroencephalogram exhibited moderate diffusion abnormality. The patient responded well to steroid impulse treatment and sodium supplement therapy, and did not recur during the follow-up. Conclusions Here we report the first AE characterized by positive LGI1 and GABABR1 antibodies, as well as summarizing AE with multiple auto-antibodies reported so far, hopefully to provide experience for clinical practice.
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EEG Contribution to the Diagnosis of Antibody-Negative Autoimmune Encephalitis: A Case Report - FullText - Case Reports in Neurology 2021, Vol. 13, No. 3 - Karger Publishers

Autoimmune encephalitis (AE) is a group of inflammatory brain diseases that are characterized by prominent neuropsychiatric symptoms. Early therapeutic intervention is important for AE.Therefore, wit...
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Author Response: Clinical, Neuroimmunologic, and CSF Investigations in First Episode Psychosis | Neurology

Author Response: Clinical, Neuroimmunologic, and CSF Investigations in First Episode Psychosis | Neurology | AntiNMDA | Scoop.it
We appreciate the interest in our research.1 According to Pollak and colleagues,2 criteria of possible autoimmune psychosis (AP) are fulfilled if a patient has abrupt onset psychotic symptoms with at least one of the following: the presence of a tumor, movement disorder (dyskinesias, catatonia), adverse response to antipsychotics, “severe or disproportionate” cognitive dysfunction, decreased level of consciousness, unexplained seizures, and significant autonomic dysfunction.2 Fulfilment of these criteria should lead to additional tests such as EEG, MRI, and serum or CSF investigations. In our series of 105 patients with first episode of psychosis (FEP), 20% fulfilled these criteria but never developed AP.1 We confirm that 2 of 3 patients with anti-N-methyl-d-aspartate receptor (anti-NMDAR) encephalitis presenting with FEP did not fulfill any of these criteria, including catatonia, which is a complex syndrome with its own set of 12 criteria that include echolalia.3 Thus, catatonia and echolalia should not be used as interchangeable terms.
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Autoantibody-associated psychiatric symptoms and syndromes in adults: A narrative review and proposed diagnostic approach

Autoantibody-associated psychiatric symptoms and syndromes in adults: A narrative review and proposed diagnostic approach | AntiNMDA | Scoop.it
Autoimmune-mediated encephalitis is a disease that often encompasses psychiatric symptoms as its first clinical manifestation’s predominant and isolated characteristic. Novel guidelines even distinguish autoimmune psychosis from autoimmune encephalitis.
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Vennada's Story: Recovery from Anti-NMDA Receptor Encephalitis

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The grey zone between autoimmune encephalitis and autoimmune‐associated epilepsy - Morano - - Epilepsia Open

The grey zone between autoimmune encephalitis and autoimmune‐associated epilepsy - Morano - - Epilepsia Open | AntiNMDA | Scoop.it
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The role of dendritic cells and their interactions in the pathogenesis of antibody-associated autoimmune encephalitis | Journal of Neuroinflammation | Full Text

The role of dendritic cells and their interactions in the pathogenesis of antibody-associated autoimmune encephalitis | Journal of Neuroinflammation | Full Text | AntiNMDA | Scoop.it
Autoimmune encephalitis (AE) is an inflammatory brain disease which is frequently associated with antibodies (Abs) against cell-surface, synaptic or intracellular neuronal proteins. There is increasing evidence that dendritic cells (DCs) are implicated as key modulators in keeping the balance...
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Unraveling the enigma of new-onset refractory status epilepticus: a systematic review of aetiologies | Read by QxMD

Unraveling the enigma of new-onset refractory status epilepticus: a systematic review of aetiologies | Read by QxMD | AntiNMDA | Scoop.it
RESULTS: Four hundred and fifty records were initially identified, of which 197 were included in the review. The selected studies were retrospective case-control (n=11), case series (n=83), and case reports (n=103) and overall described 1334 patients both of paediatric and adult age. Aetiology remains unexplained in about half of the cases, representing the so-called "cryptogenic NORSE". Among adult patients without cryptogenic NORSE, the most often identified cause is autoimmune encephalitis, either non-paraneoplastic or paraneoplastic. Infections are the prevalent aetiology of paediatric non-cryptogenic NORSE. Genetic and congenital disorders can have a causative role in NORSE, and toxic, vascular, and degenerative conditions have been also described.
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Screening for pathogenic neuronal autoantibodies in serum and CSF of patients with first-episode psychosis

Screening for pathogenic neuronal autoantibodies in serum and CSF of patients with first-episode psychosis | AntiNMDA | Scoop.it
Patients with autoimmune encephalitides, especially those with antibodies to the N-methyl-d-aspartate receptor (NMDAR), often present with prominent psychosis and respond well to immunotherapies. Although most patients progress to develop various neurological symptoms, it has been hypothesised...
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Rituximab Treatment and Long-term Outcome of Patients With Autoimmune Encephalitis | Neurology Neuroimmunology & Neuroinflammation

Rituximab Treatment and Long-term Outcome of Patients With Autoimmune Encephalitis | Neurology Neuroimmunology & Neuroinflammation | AntiNMDA | Scoop.it
Immunotherapeutic strategies for GAD65-AE remain highly controversial.27 Most patients are considered to require immunotherapy, and early immunotherapy has been found to be associated with a better outcome.10,28 However, the different neurologic manifestations of SPS, CA, and LE appear to respond...
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Anti-NMDAR Encephalitis: Multidisciplinary Development of a Clinical Practice Guideline | American Academy of Pediatrics

Anti-NMDAR Encephalitis: Multidisciplinary Development of a Clinical Practice Guideline | American Academy of Pediatrics | AntiNMDA | Scoop.it
Knowledge about the diagnosis of autoimmune encephalitis (AE) is rapidly expanding. In the last 15 years, multiple new antibodies have been described. Anti-N-methyl-D-aspartate receptor (NMDAR)–antibody-mediated encephalitis, in particular, has been found to be common among teenagers and young adults1 and accounts for up to 86% of AE in patients aged <18 years.2 Other antibodies associated with AE (leucine-rich glioma-inactivated 1, contactin-associated protein-like 2, glutamic acid decarboxylase 65-kilodalton isoform, γ-aminobutyric acid A, and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) are reported in children as case reports or series and with less clear typical clinical syndromes.3–9
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Comprehensive B-Cell Immune Repertoire Analysis of Anti-NMDAR Encephalitis and Anti-LGI1 Encephalitis

Comprehensive B-Cell Immune Repertoire Analysis of Anti-NMDAR Encephalitis and Anti-LGI1 Encephalitis | AntiNMDA | Scoop.it
Anti-N-methyl-D-aspartate receptor encephalitis (anti-NMDARE) and anti-leucine-rich glioma-inactivated 1 encephalitis (anti-LGI1E) are the two most common types of antibody-mediated autoimmune encephalitis.
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Meet Ambassador Jayden Liuzza

The Foundation is very proud to introduce our first and the world’s youngest Ambassador for Anti-NMDA receptor encephalitis, Jayden Liuzza. You may remember seeing Jayden ...Read More...
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Dysfunction of the Autonomic Nervous System and its Role in the Pathogenesis of Septic Critical Illness (Review)

Dysfunction of the Autonomic Nervous System and its Role in the Pathogenesis of Septic Critical Illness (Review) | AntiNMDA | Scoop.it
Dysfunction of the autonomic nervous system (ANS) of the brain in sepsis can cause severe systemic inflammation and even death. Numerous data confirmed the role of ANS dysfunction in the occurrence, course, and outcome of systemic sepsis.
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Frontiers | Risk Factors and Brain Metabolic Mechanism of Sleep Disorders in Autoimmune Encephalitis | Immunology

Frontiers | Risk Factors and Brain Metabolic Mechanism of Sleep Disorders in Autoimmune Encephalitis | Immunology | AntiNMDA | Scoop.it
BackgroundSleep disorders (SDs) in autoimmune encephalitis (AE) have received little attention and are poorly understood. We investigated the clinical characteristics, risk factors, and cerebral metabolic mechanism of SD in AE.MethodsClinical, laboratory, and imaging data were retrospectively...
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A peculiar case of psychosis: anti-NMDAr encephalitis | International Journal of Emergency Medicine | Full Text

A peculiar case of psychosis: anti-NMDAr encephalitis | International Journal of Emergency Medicine | Full Text | AntiNMDA | Scoop.it
Background Psychosis in pregnancy is rare and could be life-threatening. It requires prompt evaluation and proper management accordingly. Anti-N-methyl-d-aspartate receptor (anti-NMDAr) encephalitis following herpes simplex virus (HSV) infection is a rare cause of psychosis during pregnancy.
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Acute Psychosis Due to Anti-N-Methyl D-Aspartate Receptor Encephalitis Following COVID-19 Vaccination: A Case Report - PMC

Acute Psychosis Due to Anti-N-Methyl D-Aspartate Receptor Encephalitis Following COVID-19 Vaccination: A Case Report - PMC | AntiNMDA | Scoop.it
Anti-N-methyl D-aspartate (NMDA) receptor (anti-NMDAR) encephalitis has been reported after SARS-CoV-2 infection, but not after SARS-CoV-2 vaccination. We report the first known case of anti-NMDAR encephalitis after SARS-CoV-2 immunization in a young ...
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Anti-NMDAR Autoantibodies Disrupt Ionotropic Receptor Signaling –

Anti-NMDAR Autoantibodies Disrupt Ionotropic Receptor Signaling – | AntiNMDA | Scoop.it
Vignesh Subramanian '24 Figure 1: The N-methyl-D-aspartate receptor (NMDAR) functions as an ion channel. N-methyl-D-aspartate receptors (NMDARs) are ligand-gated ion channels whose signaling enables higher-order functions, such as learning and memory, throughout the brain.
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A Brain on Fire: Laura's Battle with Autoimmune Encephalitis

A Brain on Fire: Laura's Battle with Autoimmune Encephalitis | AntiNMDA | Scoop.it
Laura Martin, a strong student and standout goalie at Transylvania University, hit a sudden wall as things turned worse. Diagnosis: Autoimmune Encephalitis.
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Frontiers | Case Report: Prominent Brainstem Involvement in Two Patients With Anti-CASPR2 Antibody-Associated Autoimmune Encephalitis | Immunology

Frontiers | Case Report: Prominent Brainstem Involvement in Two Patients With Anti-CASPR2 Antibody-Associated Autoimmune Encephalitis | Immunology | AntiNMDA | Scoop.it
Anti-contactin-associated protein-like 2 (CASPR2) antibody-associated autoimmune encephalitis is commonly characterized by limbic encephalitis with clinical symptoms of mental and behavior disorders, cognitive impairment, deterioration of memory, and epilepsy.
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Frontiers | Acute Psychosis Due to Anti-N-Methyl D-Aspartate Receptor Encephalitis Following COVID-19 Vaccination: A Case Report | Neurology

Frontiers | Acute Psychosis Due to Anti-N-Methyl D-Aspartate Receptor Encephalitis Following COVID-19 Vaccination: A Case Report | Neurology | AntiNMDA | Scoop.it
Anti-N-methyl D-aspartate (NMDA) receptor (anti-NMDAR) encephalitis has been reported after SARS-CoV-2 infection, but not after SARS-CoV-2 vaccination. We report the first known case of anti-NMDAR encephalitis after SARS-CoV-2 immunization in a young female presenting with acute psychosis,...
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Lauren's Healing Story (Autoimmune Encephalitis) - Phoenix Helix

Lauren's Healing Story (Autoimmune Encephalitis) - Phoenix Helix | AntiNMDA | Scoop.it
When you have a disease only recently discovered and most doctors don't know it exists, it takes strong self-advocacy to get the help you need.
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CSF Findings in Acute NMDAR and LGI1 Antibody–Associated Autoimmune Encephalitis

CSF Findings in Acute NMDAR and LGI1 Antibody–Associated Autoimmune Encephalitis | AntiNMDA | Scoop.it
CSF in antibody-defined autoimmune encephalitis (AE) subtypes shows subtype-dependent degrees of inflammation ranging from rare and often mild to frequent and often robust. AEs with NMDA receptor antibodies (NMDAR-E) and leucine-rich glioma-inactivated ...
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Physical Therapy Interventions and Outcome Measures for a Patient Diagnosed with Anti-NMDA Receptor Encephalitis

Physical Therapy Interventions and Outcome Measures for a Patient Diagnosed with Anti-NMDA Receptor Encephalitis | AntiNMDA | Scoop.it
Anti-N-methyl-D-aspartate (NMDA) receptor encephalitis is the most common cause of
autoimmune encephalitis after acute demyelinating encephalitis. Patients usually present
with acute behavioral changes, psychosis, and abnormal limb movements and can also
...
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