The Anti-NMDA Receptor Encephalitis Foundation Newsletter

The countdown continues, with only 14 days to go before the big day! We are pleased to introduce one of the two keynote speakers of … Read More

 




To determine the prevalence of cerebrospinal fluid (CSF) markers associated with inflammation (i.e., elevated white blood cell count, protein concentr……

 




Psychosomatics Volume 61, Issue 1, January–February 2020, Pages 64-69 Case Report Delirious Mania as a Neuropsychiatric Presentation in Patients With Anti–N-methyl-D-aspartate Receptor Encephalitis Author links open overlay panel Show more Cite View full text © 2019 Academy of Consultation-Liaison Psychiatry. Published by Elsevier Inc. All rights reserved.

 




Autoimmune encephalitis (AE) is a heterogeneous class of inflammatory diseases of
the brain that can present with a wide spectrum of neuropsychiatric symptoms. Patients
may be negative for CSF anti-neuronal antibodies, which can make the diagnosis of
AE challenging.

 




SHARE January 26, 2021; 96 (4) DISPUTES & DEBATES: EDITORS’ CHOICE Editors’ Note: Clinical Significance of Anti-NMDAR Concurrent With Glial or Neuronal Surface Antibodies Ariane Lewis, Steven Galetta First published January 25, 2021, DOI: https://doi.org/10.1212/WNL.0000000000011358 FULL PDF CITATION PERMISSIONS MAKE COMMENT SEE COMMENTS Downloads0 This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased. In “Clinical Significance of Anti-NMDAR Concurrent With Glial or Neuronal Surface Antibodies,” Martinez-Hernandez et al. reported that between 4% and 7.5% of patients with anti-NMDAR encephalitis have concurrent glial or neuronal surface antibodies (glial-Ab or NS-Ab). Although they found that the presence of myelin oligodendrocyte glycoprotein (MOG) or aquaporin 4 antibodies was associated with demyelinating disorders and NS-Ab was associated with medial temporal or subcortical MRI findings, a positive glial fibrillary acidic protein (GFAP) antibody was nonspecific. McKeon et al. suggested the coexistence of GFAP antibodies and their significance may have been underreported in this study as both serum and CSF testing can be imperfect and that a phenotypic clinical-radiographic presentation associated with this antibody—a steroid-responsive meningoencephalitis with a predilection for the midbrain, cerebellar white matter, hippocampus, and cortex—may have been missed. Martinez-Hernandez et al. responded that McKeon et al. (1) misunderstood the frequency of NMDAR-Ab and GFAP-Ab co-occurrence in their cohort and (2) mischaracterized the specificity of GFAP-Ab. Lancaster reinforced Martinez-Hernandez et al.’s findings, noting that clinicians must be aware that patients with anti-NMDAR encephalitis can have multiple antibodies, which may impact presentation and prognosis. Dalmau and Martinez-Hernandez further commented that patients with NMDAR-Ab who have an atypical presentation of anti-NMDAR encephalitis should prompt consideration of the possibility that the presence of NMDAR-Ab was a false positive or that there could be concurrent antibodies but that the conclusion that any particular clinical or radiologic findings are associated with any particular antibody can only be made after careful evaluation for disease specificity. In “Clinical Significance of Anti-NMDAR Concurrent With Glial or Neuronal Surface Antibodies,” Martinez-Hernandez et al. reported that between 4% and 7.5% of patients with anti-NMDAR encephalitis have concurrent glial or neuronal surface antibodies (glial-Ab or NS-Ab). Although they found that the presence of myelin oligodendrocyte glycoprotein (MOG) or aquaporin 4 antibodies was associated with demyelinating disorders and NS-Ab was associated with medial temporal or subcortical MRI findings, a positive glial fibrillary acidic protein (GFAP) antibody was nonspecific. McKeon et al. suggested the coexistence of GFAP antibodies and their significance may have been underreported in this study as both serum and CSF testing can be imperfect and that a phenotypic clinical-radiographic presentation associated with this antibody—a steroid-responsive meningoencephalitis with a predilection for the midbrain, cerebellar white matter, hippocampus, and cortex—may have been missed. Martinez-Hernandez et al. responded that McKeon et al. (1) misunderstood the frequency of NMDAR-Ab and GFAP-Ab co-occurrence in their cohort and (2) mischaracterized the specificity of GFAP-Ab. Lancaster reinforced Martinez-Hernandez et al.’s findings, noting that clinicians must be aware that patients with anti-NMDAR encephalitis can have multiple antibodies, which may impact presentation and prognosis. Dalmau and Martinez-Hernandez further commented that patients with NMDAR-Ab who have an atypical presentation of anti-NMDAR encephalitis should prompt consideration of the possibility that the presence of NMDAR-Ab was a false positive or that there could be concurrent antibodies but that the conclusion that any particular clinical or radiologic findings are associated with any particular antibody can only be made after careful evaluation for disease specificity. Footnotes Author disclosures are available upon request (journal{at}neurology.org). See letter See letter See response © 2021 American Academy of Neurology View Full Text AAN Members We have changed the login procedure to improve access between AAN.com and the Neurology journals. 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J-STAGE…

 




We welcome the study by Martinez-Hernandez et al.1 reporting antibody coexistence in anti-n-methyl-d-aspartate receptor (NMDA-R) encephalitis. The authors confirmed coexistence of aquaporin-4-IgG or myelin oligodendrocyte glycoprotein (MOG)-IgG as predictors of co-occurrence of anti-NMDA-R…

 




Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe autoimmune paraneoplastic syndrome associated with ovarian teratomas.Most patients develop neurologic symptoms, including psychosis, memory deficits, seizures, or abnormal movements, and experience abdominal pain related to ovarian…

 




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