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Updated: Jul 22, 2025

Myelin Oligodendrocyte Glycoprotein MOG35-55 Induced Experimental Autoimmune Encephalomyelitis EAE in C57BL/6 Mice
Published on: April 15, 2014
Pearls & Oy-sters: MOG-AD Meningoencephalitis With Holocord Gray Matter Predominant Myelitis
Nathan Shmuel Farkas1, Rachel Zolno2, Cristina M Gaudioso2
1From the Department of Neurology (N.S.F.), Thomas Jefferson University, Philadelphia, PA; Department of Neurology (R.Z., C.M.G., S.M.), Washington University in St. Louis School of Medicine; and Mallinckrodt Institute of Radiology (A.Y.M.), St. Louis, MO. nathan.farkas@gmail.com.
Abstract:
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) has been implicated in a wide range of CNS encephalitis and myelitis presentations. We present a previously healthy 16-year-old girl who presented with acute onset headaches that rapidly progressed to encephalopathy, flaccid paraparesis, lower extremity hyperreflexia, and urinary retention. Serial MRI brain and total spine imaging demonstrated evolving diffuse supratentorial leptomeningeal enhancement and holocord gray matter restricted T2 bright lesion without enhancement. CSF was markedly inflammatory with MOG antibody positive >1:10,000. The patient improved after empiric steroids, plasma exchange, and IVIG.
Insights
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) can cause severe brain and spinal cord inflammation. This case highlights a rapid MOGAD presentation in a teen, successfully treated with immunotherapy.
Area of Science:
- Neurology
- Immunology
- Neuroimmunology
Background:
- Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an autoimmune condition affecting the central nervous system.
- MOGAD can manifest with diverse neurological symptoms, including encephalitis and myelitis.
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