Abstract Details

Title Bilateral Cortical Cytotoxic Edema in Pediatric MOG Antibody-associated Encephalitis: A Rare Fulminant Presentation

Topic Autoimmune Neurology

Presentation(s) P1 - Poster Session 1 (8:00 AM-9:00 AM)

Poster/Presentation
Number 2-011

Objective We highlight a rare case with severe myelin oligodendrocyte glycoprotein (MOG)-
IgG-associated cerebral cortical encephalitis (CCE) presenting as bilateral cytotoxic edema.

Background MOGAD is a recognized cause of neuroinflammation, and typically presents as acute disseminated encephalomyelitis (ADEM) in children. Recently, cerebral cortical encephalitis (CCE) involving cortical gray matter inflammation has been identified as a manifestation of the disease. Cases typically present with unilateral lesions and seizures which are steroid responsive. We report the case of MOG-IgG-associated CCE in a patient who presented with bilateral cortical cytotoxic edema, refractory seizures, and critical illness. This fulminant phenotype challenges the mild clinical course and expands the spectrum of MOGAD-related cerebral cortical encephalitis.

Design/Methods NA

Results A 13 year-old male with prior history of ADEM, six years ago, presents with fever,
headache, and encephalopathy after recent otitis media. Initial workup showed leukocytosis, CSF pleocytosis, negative infectious panel, and normal CT brain. He was treated empirically for meningitis vs. recurrent encephalomyelitis with antibiotics, IVIG and steroids. During his clinical course, he developed seizures and became obtunded. Repeat CT brain revealed diffuse cerebral edema and MRI brain revealed severe bilateral cortical edema with diffusion restriction, concerning for cytotoxic edema. He was intubated and treated with hyper-osmolor therapy. CSF encephalitis panel returned negative. Serum MOG antibody returned positive (1:320). He received 5 sessions of PLEX, cyclophosphamide, and tocilizumab and was eventually extubated; however he showed limited neurological improvement

Conclusions This case highlights a rare, fulminant presentation of MOG antibody–associated disease characterized by severe encephalopathy and bilateral cortical cytotoxic edema. Recognition of this imaging pattern is crucial, as it indicates a more aggressive disease course requiring early, intensive immunotherapy. Despite prompt initiation of multiple immunomodulatory treatments, the neurological outcome in such cases can remain poor, underscoring the need for further research to understand the pathophysiology and optimize management of severe MOG-CCE variants.

Authors/Disclosures
Nora Nikprelevic, MD, MBBS (Cleveland Clinic Weston) PRESENTER	Dr. Nikprelevic has nothing to disclose.
Mikaela D. Camacho Olalla, MD (Larkin Community Hospital)	Dr. Camacho Olalla has nothing to disclose.
Claudia Francia, MD	Dr. Francia has nothing to disclose.
Sayed Z. Naqvi, MD	Dr. Naqvi has nothing to disclose.
Anuj Jayakar, MD (Neuro Network Partners)	An immediate family member of Dr. Jayakar has received personal compensation in the range of $5,000-$9,999 for serving on a Speakers Bureau for Abvie. Dr. Jayakar has received personal compensation in the range of $5,000-$9,999 for serving as an Expert Witness for Independent.
Natanya Mishal, MD (Neuro Network Partners)	Dr. Mishal has nothing to disclose.

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