Imagine being able to predict which epilepsy patients might face a tougher battle due to their condition. That’s exactly what a groundbreaking study presented at the 2025 American Epilepsy Society (AES) Annual Meeting in Atlanta has begun to uncover. Researchers have identified specific EEG and MRI biomarkers in patients with Myelin Oligodendrocyte Glycoprotein Antibody Disease (MOGAD) and co-occurring epilepsy, shedding light on potential early warning signs for refractory epilepsy—a form of the condition that’s notoriously difficult to treat. But here’s where it gets controversial: could these biomarkers not only predict severity but also revolutionize how we approach treatment for these patients? Let’s dive in.
Led by Ally Byrd, a clinical research coordinator at Ann & Robert H. Lurie Children’s Hospital in Chicago, the study analyzed 49 MOGAD-positive patients admitted between 2015 and 2025. Among them, 14 experienced seizures, with 12 meeting the criteria for epilepsy. Strikingly, 50% of these patients had seizures as their first symptom, and 28% developed status epilepticus—a life-threatening condition of prolonged seizures. This raises a critical question: Could early detection of these biomarkers prevent such severe outcomes?
MOGAD is one of several central nervous system inflammatory demyelinating diseases, alongside multiple sclerosis and aquaporin-4-positive neuromyelitis optica spectrum disorder. The study’s goal was to pinpoint EEG and MRI biomarkers, alongside MOG antibody titers and antiepileptic medications, to improve diagnosis and management for MOGAD patients with epilepsy. And this is the part most people miss: the findings suggest that certain EEG and MRI patterns could act as red flags for refractory epilepsy, potentially allowing for earlier intervention.
Here’s the breakdown: One-third of patients had normal EEGs and didn’t require long-term antiseizure medication, while another third developed refractory epilepsy. Interestingly, all patients with intractable epilepsy showed focal slowing and interictal epileptiform discharges localized to the temporal lobe. MRI scans revealed cortical lesions in the frontal and temporal lobes, deep gray matter involvement (think thalamus, hypothalamus, and insula), and abnormalities like FLAIR hyperintensities and ring-enhancing lesions. In contrast, patients without epilepsy often presented with optic neuritis or transverse myelitis.
Now, for the intriguing part: MOG antibody titers were significantly higher in patients with epilepsy compared to those without. This aligns with recent research linking high MOG titers to relapsing disease and severe phenotypes like cortical encephalitis, which carry a higher risk of seizures and disability. Byrd and her team concluded that these biomarkers could be game-changers for early immunotherapy, potentially improving long-term outcomes. But here’s the debate: How soon should we act on these biomarkers, and what’s the threshold for intervention?
As we await further research, one thing is clear: this study opens the door to more personalized and proactive epilepsy care. What’s your take? Do these findings signal a shift in how we treat MOGAD-related epilepsy, or is it too early to tell? Share your thoughts in the comments below—let’s keep the conversation going!
