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JD is supported by Instituto Carlos III-Fondo Europeo de Desarrollo Regional (FEDER) (FIS 17/00234 and PIE 16/00014), Centro de Investigacion Biomedica en Red para Enfermedades Raras (CB15/00010), a La Caixa Foundation Health Research Award, Agencia de Gestio d'Ajuts Universitaris i de Recerca (AGAUR)-Generalitat de Catalunya, and Fundacio Cellex; and also receives royalties from Athena Diagnostics for the use of anti-Ma-2 as an autoantibody test, and from Euroimmun for the use of anti-NMDA, anti-GABAB receptor, anti-GABAA receptor, anti-DPPX and anti-IgLON5 as autoantibody tests. TA is supported by Instituto Carlos III-FEDER (FIS 18-00486), a Mutua Madrilena Foundation Award (AP162572016), and Pla Estrategic de Recerca i Innovacio en Salut (PERIS; SLT006/17/00362), and has received speaker honoraria from Novartis. FL works for an academic institution which also offers commercial antibody testing. EL has received grant support from Grifols, consulted for Merck, Janssen, and the US National Vaccine Injury Compensation Program. MJT is supported by the Netherlands Organization for Scientific Research (NWO/ZonMW, Veni incentive and Memorabel programme) and the Dutch Epilepsy Foundation (project 14-19), has filed a patent for methods for typing neurological disorders and cancer, and devices for use therein, and has received research funds for serving on a scientific advisory board of MedImmune, for consultation at Guidepoint Global, an unrestricted research grant from Euroimmun, and an Erasmus MC fellowship. MRR receives royalties from Athena Diagnostics for the use of anti-Ma-2 as an autoantibody test and from Euroimmun for the use of anti-NMDA receptor as an autoantibody test. FG receives royalties from Euroimmun for the use of anti-IgLON5 as an autoantibody test. JP is supported by PERIS (LT002/16/00346). CG is supported by the Deutsche Forschungsgemeinschaft (CRC-TR 166, TP B2). FM has no competing interests.

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An update on anti-NMDA receptor encephalitis for neurologists and psychiatrists: mechanisms and models

Publicat a:Lancet Neurology. 18 (11): 1045-1057 - 2019-11-01 18(11), DOI: 10.1016/s1474-4422(19)30244-3

Autors: Dalmau, Josep; Armangue, Thais; Planaguma, Jesus; Radosevic, Ma; Mannara, Francesco; Leypoldt, Frank; Geis, Christian; Lancaster, Eric; Titulaer, Maarten J; Rosenfeld, Myrna R; Graus, Francesc

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Resum

The identification of anti-NMDA receptor (NMDAR) encephalitis about 12 years ago made it possible to recognise that some patients with rapidly progressive psychiatric symptoms or cognitive impairment, seizures, abnormal movements, or coma of unknown cause, had an autoimmune disease. In this disease, autoantibodies serve as a diagnostic marker and alter NMDAR-related synaptic transmission. At symptom onset, distinguishing the disease from a primary psychiatric disorder is challenging. The severity of symptoms often requires intensive care. Other than clinical assessment, no specific prognostic biomarkers exist. The disease is more prevalent in women (with a female to male ratio of around 8:2) and about 37% of patients are younger than 18 years at presentation of the disease. Tumours, usually ovarian teratoma, and herpes simplex encephalitis are known triggers of NMDAR autoimmunity. About 80% of patients improve with immunotherapy and, if needed, tumour removal, but the recovery is slow. Animal models have started to reveal the complexity of the underlying pathogenic mechanisms and will lead to novel treatments beyond immunotherapy. Future studies should aim at identifying prognostic biomarkers and treatments that accelerate recovery.Copyright © 2019 Elsevier Ltd. All rights reserved.

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