MRI findings in autoimmune encephalitis.

Autoimmune diseases of the nervous system Encephalitis Magnetic resonance imaging N-methyl-D-aspartate Receptors Review literature as topic

Journal

Revue neurologique
ISSN: 0035-3787
Titre abrégé: Rev Neurol (Paris)
Pays: France
ID NLM: 2984779R

Informations de publication

Date de publication:
01 Oct 2024
Historique:
received: 03 07 2024
revised: 09 08 2024
accepted: 28 08 2024
medline: 3 10 2024
pubmed: 3 10 2024
entrez: 2 10 2024
Statut: aheadofprint

Résumé

Autoimmune encephalitis encompasses a spectrum of conditions characterized by distinct clinical features and magnetic resonance imaging (MRI) findings. Here, we review the literature on acute MRI changes in the most common autoimmune encephalitis variants. In N-methyl-D-aspartate (NMDA) receptor encephalitis, most patients have a normal MRI in the acute stage. When lesions are present in the acute stage, they are typically subtle and non-specific white matter lesions that do not correspond with the clinical syndrome. In some NMDA receptor encephalitis cases, these T2-hyperintense lesions may be indicative of an NMDA receptor encephalitis overlap syndrome with simultaneous co-existence of multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD) or myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD). Encephalitis with leucine-rich glioma-inactivated 1 (LGI1)-, contactin-associated protein-like 2 (CASPR2)- or glutamic acid decarboxylase (GAD)- antibodies typically presents as limbic encephalitis (LE) with unilateral or bilateral T2/fluid attenuated inversion recovery (FLAIR) hyperintensities in the medial temporal lobe that can progress to hippocampal atrophy. Gamma aminobutyric acid-B (GABA-B) receptor encephalitis also often shows such medial temporal hyperintensities but may additionally involve cerebellar lesions and atrophy. Gamma aminobutyric acid-A (GABA-A) receptor encephalitis features multifocal, confluent lesions in cortical and subcortical areas, sometimes leading to generalized atrophy. MRI is unremarkable in most patients with immunoglobulin-like cell adhesion molecule 5 (IgLON5)-disease, while individual case reports identified T2/FLAIR hyperintense lesions, diffusion restriction and atrophy in the brainstem, hippocampus and cerebellum. These findings highlight the need for MRI studies in patients with suspected autoimmune encephalitis to capture disease-specific changes and to exclude alternative diagnoses. Ideally, MRI investigations should be performed using dedicated autoimmune encephalitis imaging protocols. Longitudinal MRI studies play an important role to evaluate potential relapses and to manage long-term complications. Advanced MRI techniques and current research into imaging biomarkers will help to enhance the diagnostic accuracy of MRI investigations and individual patient outcome prediction. This will eventually enable better treatment decisions with improved clinical outcomes.

Identifiants

pubmed: 39358087
pii: S0035-3787(24)00590-3
doi: 10.1016/j.neurol.2024.08.006
pii:
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 The Author(s). Published by Elsevier Masson SAS.. All rights reserved.

Auteurs

T J Hartung (TJ)

Charité - Universitätsmedizin Berlin, Department of Neurology and Experimental Neurology, Berlin, Germany.

F Bartels (F)

Charité - Universitätsmedizin Berlin, Department of Neurology and Experimental Neurology, Berlin, Germany; Berlin Institute of Health at Charité - Universitätsmedizin Berlin, Berlin, Germany; Humboldt-Universität zu Berlin, Berlin School of Mind and Brain, Berlin, Germany.

J Kuchling (J)

Charité - Universitätsmedizin Berlin, Department of Neurology and Experimental Neurology, Berlin, Germany.

S Krohn (S)

Charité - Universitätsmedizin Berlin, Department of Neurology and Experimental Neurology, Berlin, Germany; Humboldt-Universität zu Berlin, Berlin School of Mind and Brain, Berlin, Germany.

J Leidel (J)

Charité - Universitätsmedizin Berlin, Department of Neurology and Experimental Neurology, Berlin, Germany.

M Mantwill (M)

Charité - Universitätsmedizin Berlin, Department of Neurology and Experimental Neurology, Berlin, Germany.

K Wurdack (K)

Charité - Universitätsmedizin Berlin, Department of Neurology and Experimental Neurology, Berlin, Germany.

S Yogeshwar (S)

Charité - Universitätsmedizin Berlin, Department of Neurology and Experimental Neurology, Berlin, Germany; Charité - Universitätsmedizin Berlin, Einstein Center for Neurosciences Berlin, Berlin, Germany.

M Scheel (M)

Charité - Universitätsmedizin Berlin, Department of Neuroradiology, Berlin, Germany.

C Finke (C)

Charité - Universitätsmedizin Berlin, Department of Neurology and Experimental Neurology, Berlin, Germany; Humboldt-Universität zu Berlin, Berlin School of Mind and Brain, Berlin, Germany; Charité - Universitätsmedizin Berlin, Einstein Center for Neurosciences Berlin, Berlin, Germany. Electronic address: carsten.finke@charite.de.

Classifications MeSH