Authors :
Presenting Author: Leen Younis, MD – Lurie Childrens Hospital
Priyamvada Tatachar, MBBS, MD – Ann & Robert H. Lurie Children’s Hospital of Chicago
Kavita Thakkar, MD – Lurie Children's Hospital
Aadi Rao, MD candidate – Lurie Children's Hospital
Enrique Rojas, CCRC – Ann and Robert H Lurie Children's Hospital of Chicago
Sofia Mirshed, MBA, CCRP – Ann & Robert H. Lurie Children's Hospital of Chicago
Alexandra Byrd, CCRC – Lurie Children's Hospital
Rationale:
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a demyelinating disorder in which seizures occur in approximately 10% of patients and are a common first presentation of the disease. Despite the growing recognition of seizures in MOGAD, the neurophysiological and neuroimaging correlates remain poorly characterized. This research aims to characterize EEG and MRI biomarkers that may assist in diagnosis and management of patients with MOGAD and epilepsy.Methods:
Retrospective chart review of 49 patients who tested positive for MOG antibody positive who were admitted to Lurie Children’s Hospital in Chicago from Jan 1st 2015 - June 2nd 2025. Data were collected looking at seizure semiology, EEG findings (background, interictal and ictal findings) and MRI findings, MOGAD titers and antiepileptic medications. Results:
Among the 49 MOG-positive patients, 14 experienced seizures, with 12 meeting criteria for epilepsy. Seizures were the initial presentation in 7 out of 14 (50%) patients, and 4 (28%) presented in status epilepticus. Notably, 4 patients (33%) had normal EEGs and did not require long-term ASM treatment, whereas 4 (33%) developed refractory epilepsy. All patients with intractable epilepsy demonstrated focal slowing and interictal epileptiform discharges originating from a single lobe—specifically, the temporal lobe.
MRI findings in the epilepsy group commonly included cortical lesions in the frontal and temporal lobes, deep gray matter involvement (including thalamus, hypothalamus, and insula), FLAIR hyperintensities, ring-enhancing lesions, and leptomeningeal enhancement. In contrast, patients without epilepsy most frequently showed optic neuritis (14/36, 38.8%) and transverse myelitis (12/36, 33%) at presentation. Persistent MRI abnormalities were observed in 3 of 4 patients (75%) with refractory epilepsy on follow-up imaging.
MOG antibody titers were higher in patients with epilepsy (range 1:80–1:10,000; median 1:000) compared to those without epilepsy (range 1:10–1:1000; mean 1:160).
Conclusions:
This study highlights the characteristics of patients with MOGAD with diagnosis of epilepsy. Patients presenting with refractory status epilepticus, diffuse EEG slowing with focal interictal discharges, and MRI findings involving cortical and deep structures may represent a more severe disease phenotype. 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.Funding: None