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Autoimmune Encephalitis and Its Relation to Infection

  • Arun Venkatesan
  • David R. Benavides
Infection (ML Solbrig, Section Editor)
Part of the following topical collections:
  1. Topical Collection on Infection

Abstract

Encephalitis, an inflammatory condition of the brain that results in substantial morbidity and mortality, has numerous causes. Over the past decade, it has become increasingly recognized that autoimmune conditions contribute significantly to the spectrum of encephalitis causes. Clinical suspicion and early diagnosis of autoimmune etiologies are of particular importance due to the need for early institution of immune suppressive therapies to improve outcome. Emerging clinical observations suggest that the most commonly recognized cause of antibody-mediated autoimmune encephalitis, anti-N-methyl-d-aspartate (NMDA) receptor encephalitis, may in some cases be triggered by herpes virus infection. Other conditions such as Rasmussen’s encephalitis (RE) and febrile infection-related epilepsy syndrome (FIRES) have also been posited to be autoimmune conditions triggered by infectious agents. This review focuses on emerging concepts in central nervous system autoimmunity and addresses clinical and mechanistic findings linking autoimmune encephalitis and infections. Particular consideration will be given to anti-NMDA receptor encephalitis and its relation to herpes simplex encephalitis.

Keywords

Autoimmune encephalopathy CNS autoimmunity Anti-NMDA receptor antibodies FIRES Rasmussen’s syndrome Molecular mimicry 

Notes

Acknowledgments

David R. Benavides is supported by NINDS T32 training grant in neuroimmunology and neurological infectious disease (T32NS069351).

Arun Venkatesan receives support from the National Institutes of Health, Maryland Stem Cell Research Fund, and Accelerated Cure Project for Multiple Sclerosis.

Compliance with Ethics Guidelines

Conflict of Interest

Arun Venkatesan and David R. Benavides declare that they have no conflict of interest.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by any of the authors.

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© Springer Science+Business Media New York 2015

Authors and Affiliations

  1. 1.Johns Hopkins Encephalitis Center, Department of NeurologyJohns Hopkins University School of MedicineBaltimoreUSA

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