AES Poster Lays Insights Into EEG and MRI Biomarkers of MOGAD-Related Epilepsy

A recently presented retrospective chart review study provided a greater understanding about the EEG and MRI characteristics of patients with myelin oligodendrocyte glycoprotein antibody disease (MOGAD) with co-occurring epilepsy. Among the takeaways, investigators concluded that those with refractory status epilepticus, characteristic EEG slowing, and cortical deep MRI abnormalities may represent a more severe phenotype in whom these features could serve as early biomarkers of refractory epilepsy.¹

Presented at 2025 American Epilepsy Society (AES) Annual Meeting, held December 5-9, in Atlanta, Georgia, the analysis included 49 patients who tested positive for MOG antibody positive who were admitted to Lurie Children’s Hospital in Chicago from January 2015 to June 2025. Among those included, 14 experienced seizures (12 meeting criteria for epilepsy), with seizures as the initial presentation in 7 (50%) and status epilepticus in 4 (28%).

Seizure is one of the manifestations of central nervous system inflammatory demyelinating diseases, which mainly include multiple sclerosis, aquaporin-4-positive neuromyelitis optica spectrum disorder, and MOGAD. Led by Ally Bryd, clinical research coordinator lead at the Ann & Lurie Children’s Hospital, the study aimed to characterize EEG and MRI biomarkers along with MOGAD titers and antiepileptic medications to better assist in the diagnosis and management of patients with MOGAD with co-existing epilepsy.

In the study, one-third (33%; n = 4) of patients had normal EEGs and did not require long-term antiseizure (ASM) treatment, whereas another one-third (33%; n = 4) developed refractory epilepsy. Of note, all patients with intractable epilepsy showed focal slowing and interictal epileptiform discharges arising from a single region, consistently localized to the temporal lobe.

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Among those who met criteria for epilepsy, MRI commonly showed cortical lesions in the frontal and temporal lobes, involvement of deep gray structures such as the thalamus, hypothalamus, and insula, as well as FLAIR hyperintensities, ring-enhancing lesions, and leptomeningeal enhancement. By comparison, those without epilepsy most often presented with optic neuritis (14/36, 38.8%) or transverse myelitis (12/36, 33%). Among patients with refractory epilepsy, follow-up imaging revealed persistent MRI abnormalities in 3 of 4 cases (75%).

In the study, MOG antibody titers were higher in patients with epilepsy (range: 1:80-1:10,000; median, 1:000) compared with those without epilepsy (range: 1:10-1:1000; mean, 1:160). This was significant, as recent biomarker reviews have noted that persistently positive or very high MOG titers and intrathecal MOG-IgG production are associated with relapsing disease and “refractory” phenotypes such as cortical encephalitis and severe myelitis, which themselves carry higher seizure and disability risk.²

Byrd et al concluded that, "These findings suggest that higher MOG titers and specific EEG/MRI abnormalities may serve as early biomarkers of refractory epilepsy. Early identification of these markers could support prompt initiation of immunotherapy, potentially improving long-term seizure control and neurological outcomes."

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REFERENCES
1. Younis L, Tatachar P, Thakkar K, et al. EEG and MRI Biomarkers in patients diagnosed with Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) with Epilepsy. Presented at: 2025 AES Annual Meeting; December 5-9; Atlanta, GA. ABSTRACT 2.247
2. Sapana T, Zhuo Z. Biomarkers for diagnosis and prognosis of myelin oligodendrocyte glycoprotein antibody-associated disease - review article. Multiple Sclerosis & Neuroimmun. 2025;16. doi:10.3389/fimmu.2025.1594960