Related Experiment Video
Updated: Jul 16, 2026

Induction and Clinical Scoring of Chronic-Relapsing Experimental Autoimmune Encephalomyelitis
Published on: July 4, 2007
MRI cortical thickness in paediatric auto-immune encephalitis and acute disseminated encephalomyelitis
Charly H A Billaud1, Daniel Griffiths-King2, Evangeline Wassmer3
1College of Health & Life Sciences & Aston Institute of Health and Neurodevelopment, Aston University, Birmingham, UK; Psychology, School of Social Sciences, Nanyang Technological University, Singapore.
Objective:
Paediatric autoimmune encephalitis and acute disseminated encephalomyelitis (ADEM) are neuroinflammatory disorders that can cause acute MRI abnormalities. Recent analyses suggest brain volume reductions months to years after disease onset. This study aimed to verify whether decreased gray matter thickness would also be observed in whole-brain cortical thickness as well as in temporal polar and orbitofrontal cortices.
Methods:
A cohort of children previously diagnosed with autoimmune encephalitis (including anti-NMDA encephalitis and ADEM) were recruited at least two years after initial presentation and a cohort of typically developing children with no known neurological conditions. Cortical thickness across the whole-brain and in each region-of-interest was measured from T1w MRI scans using Freesurfer.
Results:
MRI scans from 12 children with autoimmune encephalitis (mean age = 10.5; 8F:4M) and 48 controls (mean age = 10.7; 23F 25M) were analysed. The autoimmune encephalitis group had lower cortical thickness in a cluster covering the top part of the left superior occipital gyrus and the bottom part of the left superior parietal lobule (cluster size = 681.55 mm2; corrected cluster-wise p = .00459; cluster-wise Cohen's d = -8.3773). No multivariate effect on the cortical thickness of the regions-of-interest was found (Roy's Largest Root = .095, F(df) = 1.207(4); p = .319; partial η2 = .087). A small univariate effect was observed, with autoimmune encephalitis predicting lower left orbitofrontal thickness (F = 4.407, p = .040, Partial η2 = .075).
Interpretation:
Children with autoimmune encephalitis may be subject to local cortical thinning in the long term.
Insights
Children with autoimmune encephalitis may experience long-term cortical thinning. This study found reduced gray matter thickness in specific brain regions years after disease onset, highlighting potential chronic neuroinflammatory effects.
Area of Science:
- Neuroscience
- Radiology
- Pediatric Neurology
Background:
- Paediatric autoimmune encephalitis and acute disseminated encephalomyelitis (ADEM) are neuroinflammatory disorders.
- These conditions can lead to acute MRI abnormalities and are increasingly associated with long-term brain volume reductions.
Purpose of the Study:
- To investigate long-term changes in cortical thickness in children diagnosed with autoimmune encephalitis (including anti-NMDA encephalitis and ADEM).
- To determine if decreased gray matter thickness is present in whole-brain cortical thickness, temporal polar, and orbitofrontal cortices years after disease onset.
Main Methods:
- A cohort of children with a history of autoimmune encephalitis (at least two years post-diagnosis) and a control group of typically developing children were recruited.
- Cortical thickness was measured from T1w MRI scans using Freesurfer for whole-brain analysis and specific regions of interest.
Main Results:
- MRI analysis of 12 children with autoimmune encephalitis and 48 controls revealed significantly lower cortical thickness in a cluster encompassing parts of the left superior occipital gyrus and left superior parietal lobule.
- No significant multivariate effect was found on the cortical thickness of the specific regions of interest, although a univariate effect indicated lower left orbitofrontal thickness in the autoimmune encephalitis group.
Conclusions:
- Children with autoimmune encephalitis may experience localized cortical thinning as a long-term consequence of the disease.
- These findings suggest persistent structural brain changes following pediatric neuroinflammatory disorders.
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