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Author Notes:

Anna-Marieta Moise, MD, 890 Hendersonville Rd Suite 200, Asheville, NC 28803, U.S.A. Email: annamo2@gmail.com

The authors specially thank the EEG technicians from Emory, Yale, and Massachusetts General Hospital, with Shanaz Merchant from the Emory University for technical support. They also thank all the physicians from the Emory University, Massachusetts General, and Yale University who helped with this project. They also thank the CCMERC for the advisory support for this project.

The authors have no conflicts of interest to disclose.


Research Funding:

Supported by the National Center for Advancing Translational Sciences of the National Institutes of Health under Award Number UL1TR000454. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.


  • Science & Technology
  • Life Sciences & Biomedicine
  • Clinical Neurology
  • Neurosciences
  • Neurosciences & Neurology
  • Continuous EEG
  • Autoimmune encephalitis
  • Electrographic findings in autoimmune encephalitis
  • Encephalitis
  • Anti-NMDA-receptor encephalitis
  • Limbic encephalitis
  • Hashimoto encephalopathy

Continuous EEG Findings in Autoimmune Encephalitis

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Journal Title:



Volume 38, Number 2


, Pages 124-129

Type of Work:

Article | Post-print: After Peer Review


Purpose:Autoimmune encephalitis (AE) is a cause of new-onset seizures, including new-onset refractory status epilepticus, yet there have been few studies assessing the EEG signature of AE.Methods:Multicenter retrospective review of patients diagnosed with AE who underwent continuous EEG monitoring.Results:We identified 64 patients (male, 39%; white, 49%; median age, 44 years); of whom, 43 (67%) were antibody-proven AE patients. Of the patients with confirmed antibody AE, the following were identified: N-methyl-D-aspartate receptor (n = 17, 27%), voltage-gated potassium channel (n = 16, 25%), glutamic acid decarboxylase (n = 6, 9%), and other (n = 4, 6%). The remaining patients were classified as probable antibody-negative AE (n = 11, 17%), definite limbic encephalitis (antibody-negative) (n = 2, 3%), and Hashimoto encephalopathy (n = 8, 13%). Fifty-three percent exhibited electrographic seizures. New-onset refractory status epilepticus was identified in 19% of patients. Sixty-three percent had periodic or rhythmic patterns; of which, 38% had plus modifiers. Generalized rhythmic delta activity was identified in 33% of patients. Generalized rhythmic delta activity and generalized rhythmic delta activity plus fast activity were more common in anti-N-methyl-D-aspartate AE (P = 0.0001 and 0.0003, respectively). No other periodic or rhythmic patterns exhibited AE subtype association. Forty-two percent had good outcome on discharge. Periodic or rhythmic patterns, seizures, and new-onset refractory status epilepticus conferred an increased risk of poor outcome (OR, 6.4; P = 0.0012; OR, 3; P = 0.0372; OR, 12.3; P = 0.02, respectively).Conclusion:Our study confirms a signature EEG pattern in anti-N-methyl-D-aspartate AE, termed extreme delta brush, identified as generalized rhythmic delta activity plus fast activity in our study. We found no other pattern association with other AE subtypes. We also found a high incidence of seizures among patients with AE. Finally, periodic or rhythmic patterns, seizures, and new-onset refractory status epilepticus conferred an increased risk of poor outcome regardless of AE subtype.

Copyright information:

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (https://creativecommons.org/licenses/by-nc/4.0/rdf).
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