A groundbreaking study sheds light on the complex relationship between MOGAD, epilepsy, and potential biomarkers for improved treatment. But here's where it gets intriguing: it suggests that specific EEG and MRI markers could be the key to identifying and managing a severe form of epilepsy associated with MOGAD.
The study, presented at the 2025 American Epilepsy Society (AES) Annual Meeting, analyzed 49 patients with MOG antibody positivity admitted to a Chicago hospital over a decade. Researchers found that 14 patients experienced seizures, with epilepsy criteria met in 12 cases. Notably, seizures were the initial presentation in half of these cases, and status epilepticus occurred in nearly a third.
MOGAD, a central nervous system inflammatory demyelinating disease, can manifest as seizures. The study, led by Ally Bryd, sought to explore EEG and MRI biomarkers alongside MOGAD titers and antiepileptic medications to enhance diagnosis and treatment for MOGAD patients with epilepsy.
A fascinating finding emerged: 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 exhibited focal slowing and interictal epileptiform discharges from a single region, specifically the temporal lobe.
MRI scans revealed cortical lesions in the frontal and temporal lobes, deep gray structure involvement, and various abnormalities in patients with epilepsy. Optic neuritis and transverse myelitis were more common in those without epilepsy. In refractory epilepsy cases, follow-up imaging showed persistent MRI abnormalities in most cases.
And this is the part most people miss: MOG antibody titers were significantly higher in patients with epilepsy compared to those without. This is crucial because persistently elevated MOG titers are linked to relapsing disease and severe phenotypes like cortical encephalitis and myelitis, which increase seizure and disability risks.
The researchers suggest that higher MOG titers and specific EEG/MRI abnormalities could be early indicators of refractory epilepsy. Identifying these markers early may enable prompt immunotherapy, potentially enhancing seizure control and neurological outcomes.
This study offers a promising direction for epilepsy management in MOGAD patients, but it also raises questions. Could these biomarkers be the missing link to predicting and preventing severe epilepsy cases? What further research is needed to validate these findings and translate them into clinical practice? Share your thoughts in the comments below!
