AI Article Synopsis

  • Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is a recently recognized autoimmune disorder affecting the central nervous system, with specific antibodies present in patients; this study investigates leptomeningeal enhancement (LME) in children with MOG antibody-associated encephalitis (MOG-E) using MRI imaging.
  • An analysis of MRI images and clinical symptoms from 78 children revealed that LME was common, appearing in 54.5% of cases and serving as a significant early indicator of MOG-E, particularly linked to the presence of lesions in specific brain areas.
  • The findings suggest that LME could be an important biomarker for early diagnosis in MOG-E, which could help guide

Article Abstract

Background: Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is a newly defined autoimmune inflammatory demyelinating central nervous system (CNS) disease characterized by antibodies against MOG. Leptomeningeal enhancement (LME) on contrast-enhanced fluid-attenuated inversion recovery (CE-FLAIR) images has been reported in patients with other diseases and interpreted as a biomarker of inflammation. This study retrospectively analyzed the prevalence and distribution of LME on CE-FLAIR images in children with MOG antibody-associated encephalitis (MOG-E). The corresponding magnetic resonance imaging (MRI) features and clinical manifestations are also presented.

Methods: The brain MRI images (native and CE-FLAIR) and clinical manifestations of 78 children with MOG-E between January 2018 and December 2021 were analyzed. Secondary analyses evaluated the relationship between LME, clinical manifestations, and other MRI measures.

Results: Forty-four children were included, and the median age at the first onset was 70.5 months. The prodromal symptoms were fever, headache, emesis, and blurred vision, which could be progressively accompanied by convulsions, decreased level of consciousness, and dyskinesia. MOG-E showed multiple and asymmetric lesions in the brain by MRI, with varying sizes and blurred edges. These lesions were hyperintense on the T2-weighted and FLAIR images and slightly hypointense or hypointense on the T1-weighted images. The most common sites involved were juxtacortical white matter (81.8%) and cortical gray matter (59.1%). Periventricular/juxtaventricular white matter lesions (18.2%) were relatively rare. On CE-FLAIR images, 24 (54.5%) children showed LME located on the cerebral surface. LME was an early feature of MOG-E ( = 0.002), and cases without LME were more likely to involve the brainstem ( = 0.041).

Conclusion: LME on CE-FLAIR images may be a novel early marker among patients with MOG-E. The inclusion of CE-FLAIR images in MRI protocols for children with suspected MOG-E at an early stage may be useful for the diagnosis of this disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10318903PMC
http://dx.doi.org/10.3389/fimmu.2023.1152235DOI Listing

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