MOG Antibody Disease: A New Brain Condition Distinct from MS and NMO

MOG Antibody Disease (MOGAD) — caused by antibodies against myelin oligodendrocyte glycoprotein — has emerged in the last decade as a distinct autoimmune demyelinating condition of the CNS, separable from both Multiple Sclerosis (MS) and AQP4-positive NMO. It disproportionately affects children and young adults, has a characteristic pattern of involvement, and — crucially — has a different treatment response to MS medications. Misclassifying MOGAD as MS can lead to ineffective treatment.

Clinical Presentations

MOGAD presents as: Optic neuritis: Often bilateral (unlike MS optic neuritis, which is usually unilateral); severe pain with eye movement; vision loss that typically recovers well. ADEM-like presentation: Particularly in children — encephalopathy with multifocal lesions, seizures, and behavioural change following a viral illness. Responds well to steroids. Transverse myelitis: Less longitudinally extensive than NMO-TM — often conus involvement causing bladder and bowel problems. CRION (Chronic Relapsing Inflammatory Optic Neuropathy): Steroid-dependent optic neuritis that relapses when steroids are tapered. Cortical encephalitis: A specific syndrome with seizures, headache, and FLAIR cortical signal changes.

Key Differences from MS

MOGAD: typically good recovery from attacks; often bilateral optic neuritis; normal brain MRI between attacks (in many); anti-MOG antibody positive; AQP4 negative; MS drugs may not prevent attacks. MS: typically unilateral optic neuritis; accumulating brain lesions; oligoclonal bands in CSF; specific disease-modifying therapies.

Treatment

Acute attacks: IV methylprednisolone; plasma exchange for non-responders. Relapse prevention: low-dose maintenance prednisolone; azathioprine; mycophenolate; rituximab for refractory cases. Anti-MOG antibody testing is now available in Hyderabad. Sri Anand CNC, Chanda Nagar, Hyderabad. Call +91 90633 66983.