Autoimmune Encephalitis MRI
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Julinka Auta Fernandes
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Autoimmune Encephalitis Microchapters |
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Differentiating Autoimmune Encephalitis from Other Conditions |
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Diagnosis |
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Autoimmune Encephalitis On the Web |
Overview
Autoimmune encephalitis may produce focal or multifocal abnormalities on magnetic resonance imaging (MRI), but a normal brain MRI does not exclude the disease. Imaging can support an inflammatory diagnosis, identify the anatomical pattern, and reveal alternative explanations for the presentation. Findings must be interpreted alongside the clinical course and other investigations.[1]
Medial temporal signal abnormality is a recognizable pattern of autoimmune limbic encephalitis. However, autoimmune encephalitis can also affect the cortex, subcortical regions, basal ganglia, diencephalon, or brainstem. An imaging pattern alone does not identify the responsible antibody.[2]
Key MRI Findings in Autoimmune Encephalitis
MRI Acquisition
In autoimmune encephalitis, brain MRI should generally be obtained before and after gadolinium when clinically appropriate. Contrast use and any need for sedation require individual assessment.
A useful protocol includes:
- T2-weighted (transverse relaxation-weighted) imaging and fluid-attenuated inversion recovery (FLAIR) imaging to assess abnormal tissue signal and swelling.
- T1-weighted (longitudinal relaxation-weighted) imaging, preferably with high-resolution three-dimensional acquisition, for anatomy and assessment of volume loss.
- Diffusion-weighted imaging (DWI) with apparent diffusion coefficient (ADC) maps to assess true diffusion restriction.
- Susceptibility-weighted imaging (SWI) or an appropriate susceptibility-sensitive sequence to assess blood products.
- Postcontrast T1-weighted imaging to evaluate parenchymal or meningeal enhancement.
Coronal images through the hippocampi help assess subtle medial temporal abnormalities.[3]
Limbic Pattern
In autoimmune encephalitis with limbic involvement, MRI may show:
- Increased T2/FLAIR signal in the hippocampus and amygdala.
- Unilateral or bilateral medial temporal involvement, which may be asymmetric.
- Swelling during the active phase.
- Subsequent hippocampal volume loss or sclerosis in some patients.[4]
Bilateral medial temporal abnormalities do not independently establish autoimmune limbic encephalitis. Under the 2016 consensus criteria, this imaging finding must occur with the appropriate subacute limbic syndrome, supporting cerebrospinal fluid (CSF) inflammation or temporal abnormalities on electroencephalography (EEG), and reasonable exclusion of alternative causes. A unilateral abnormality does not satisfy that specific MRI criterion, although antibody-defined autoimmune encephalitis can still be diagnosed through the appropriate pathway.[5]
Initial and Follow-Up MRI
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Patterns Associated With Selected Antibodies
In autoimmune encephalitis, the following MRI associations can help organize the differential diagnosis, but they are neither obligatory nor antibody-specific.
| Antibody-associated disease | Possible MRI pattern |
|---|---|
| N-methyl-D-aspartate receptor (NMDAR) antibody encephalitis | MRI is frequently normal. Abnormal studies may show limbic or extralimbic lesions rather than one consistent diagnostic pattern.[7][4] |
| Leucine-rich glioma-inactivated protein 1 (LGI1) antibody encephalitis | Medial temporal T2/FLAIR hyperintensity and hippocampal swelling; hippocampal atrophy or sclerosis may develop on follow-up.[4] |
| Contactin-associated protein-like 2 (CASPR2) antibody encephalitis | Medial temporal abnormalities may occur with a limbic presentation; imaging can also be normal.[8] |
| Gamma-aminobutyric acid type B receptor (GABA-B receptor) antibody encephalitis | A medial temporal or limbic pattern may be present.[8] |
| Gamma-aminobutyric acid type A receptor (GABA-A receptor) antibody encephalitis | Multifocal cortical and subcortical T2/FLAIR-hyperintense lesions.[8] |
| Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) antibody encephalitis | A limbic pattern with medial temporal abnormalities may occur.[3] |
| Paraneoplastic antigen Ma2 antibody-associated encephalitis | Limbic, diencephalic, or brainstem involvement may occur.[3] |
| Collapsin response-mediator protein 5 (CRMP5; also called CV2) antibody-associated encephalitis | Striatal or other basal ganglia involvement may occur.[3] |
Enhancement and Diffusion
In autoimmune encephalitis, contrast enhancement may be absent or mild and patchy. Extensive or unusually intense enhancement requires careful assessment for alternative explanations. Cortical diffusion restriction may occur, including in association with seizures.[2]
True restriction should be assessed using ADC maps rather than DWI brightness alone. Restriction is not a universal autoimmune encephalitis finding; its presence does not exclude the disease, as restricted diffusion has been documented in antibody-confirmed cases.[4]
Related Inflammatory and Demyelinating Patterns
In the evaluation of suspected autoimmune encephalitis, some MRI appearances suggest related inflammatory disorders rather than a typical neuronal antibody encephalitis:
- Glial fibrillary acidic protein (GFAP) astrocytopathy: radial perivascular enhancement can be a useful clue, but is not independently diagnostic.[8]
- Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease: cortical T2/FLAIR abnormalities may accompany an encephalitic presentation. A prominent demyelinating pattern should prompt assessment for an overlapping or alternative disorder.[1]
Spinal MRI should be obtained when symptoms or examination findings suggest spinal cord involvement, rather than routinely in every patient.[1]
Important MRI Mimics
In autoimmune encephalitis assessment, MRI abnormalities must be distinguished from:
- Herpes simplex encephalitis, which may involve temporal and insular regions and can show hemorrhagic changes.
- Peri-ictal abnormalities related to recent seizures or status epilepticus.
- Ischemic stroke.
- Creutzfeldt-Jakob disease.
- Neoplasm, including infiltrative lesions.
Temporal signal abnormality alone cannot distinguish these conditions. Distribution, diffusion, susceptibility findings, enhancement, interval change, and clinical context should be considered together.[2][5]
Repeat MRI and Follow-Up
In autoimmune encephalitis, repeat brain MRI should be considered when the initial examination is normal but clinical suspicion remains strong, or when the course is unexplained by the initial findings.[1]
Follow-up can demonstrate resolution of signal abnormality and swelling, persistent lesions, or hippocampal atrophy and sclerosis. These changes should be interpreted alongside symptoms and seizure activity; an imaging change alone should not be treated as proof of relapse or treatment failure.[4]
MRI findings have variable prognostic value. In a multicenter pediatric NMDAR antibody encephalitis cohort, only 34% of patients had abnormal brain MRI, and associations between lesion location and outcome were sensitive to the statistical model. MRI should therefore not be used alone to predict an individual patient's recovery.[7]
References
- ↑ 1.0 1.1 1.2 1.3 Hahn C, Budhram A, Alikhani K, et al. Canadian Consensus Guidelines for the Diagnosis and Treatment of Autoimmune Encephalitis in Adults. Canadian Journal of Neurological Sciences. 2024;51(6):734–754. doi:10.1017/cjn.2024.16. PMID:38312020.
- ↑ 2.0 2.1 2.2 Abboud H, Probasco JC, Irani S, et al. Autoimmune encephalitis: proposed best practice recommendations for diagnosis and acute management. Journal of Neurology, Neurosurgery & Psychiatry. 2021;92(7):757–768. doi:10.1136/jnnp-2020-325300. PMID:33649022.
- ↑ 3.0 3.1 3.2 3.3 Sanvito F, Pichiecchio A, Paoletti M, et al. Autoimmune encephalitis: what the radiologist needs to know. Neuroradiology. 2024;66(5):653–675. doi:10.1007/s00234-024-03318-x. PMID:38507081.
- ↑ 4.0 4.1 4.2 4.3 4.4 Seery N, Beech P, Wesselingh R, et al.; Australian Autoimmune Encephalitis Consortium. Acute and longitudinal magnetic resonance imaging abnormalities in antibody-mediated encephalitis. Brain Communications. 2026;8(3):fcag193. doi:10.1093/braincomms/fcag193. PMID:42318510.
- ↑ 5.0 5.1 Graus F, Titulaer MJ, Balu R, et al. A clinical approach to diagnosis of autoimmune encephalitis. Lancet Neurology. 2016;15(4):391–404. doi:10.1016/S1474-4422(15)00401-9. PMID:26906964.
- ↑ 6.0 6.1 Mohamed K. Radiopaedia case rID: 160412. Radiopaedia.org.
- ↑ 7.0 7.1 Gombolay G, Brenton JN, Yang JH, et al. MRI Features and Their Association With Outcomes in Children With Anti-NMDA Receptor Encephalitis. Neurology: Neuroimmunology & Neuroinflammation. 2023;10(4):e200130. doi:10.1212/NXI.0000000000200130. PMID:37236807.
- ↑ 8.0 8.1 8.2 8.3 Hartung TJ, Kuchling J, Finke C. The role of brain MRI in autoimmune encephalitis. Current Opinion in Neurology. 2026;39(3):332–340. doi:10.1097/WCO.0000000000001484. PMID:41947644.