Working Diagnosis:
Myelin oligodendrocyte glycoprotein antibody associated disease (MOGAD)

Treatment:
He was admitted to the hospital and treated with high dose IV steroids for 5 days, with dramatic clinical improvement in his vision and ocular pain. His previously noted optic disc edema resolved. He was subsequently started on Rituximab to minimize his risk of disease recurrence.

Outcome:
The athlete had full recovery of symptoms without any relapse or new attacks. He did not participate in the remainder of fall football. He was cleared by both ophthalmology and neurology for full return-to-play and returned to football for the spring season.

Author's Comments:
Myelin oligodendrocyte glycoprotein (MOG), a protein on the surface of oligodendrocytes, was once considered as a potential antibody target in multiple sclerosis (MS), but in 2007 was identified as a separate demyelinating disease. The Overall incidence of MOGAD is largely unknown, though the median age onset appears to be between 20-30 years of age. Patients typically present with optic neuritis, acute disseminated encephalopathy, or transverse myelitis and the disease course can be monophasic or recurrent. Acute attacks are treated with high dose IV steroids over 5 days and can be augmented with IVIG or plasma exchange. Approximately 50% of patients will experience recurrent disease. Immunosuppression can help minimize recurrence.

Editor's Comments:
MOGAD is an autoimmune, demyelinating disease affecting the CNS, causing optic neuritis, transverse myelitis, and/or encephalomyelitis. This presentation can appear clinically similar to Multiple Sclerosis (MS), Neuromyelitis Optica Spectrum Disorder (NMOSD), or Acute Disseminated Encephalomyelitis (ADEM). One study found 40% of those with antibody-negative NMSOD ultimately had MOGAD. This condition preferentially affects adults in their 20s-30s, but can occur in children and in older adults. Physicians should consider serum testing for Myelin oligodendrocyte glycoprotein (MOG)-IgG when patients present with symptoms consistent with MS or NMSOD, particularly when initial work-ups are not consistent with these more common diseases.

There are no randomized control trials for the treatment of MOGAD, and current therapies are based on treatments for similar diseases of NMSOD and MS. While use of immunomodulators like rituximab have proven very effective for NMSOD, its efficacy is less well documented in MOGAD. Further study is needed to determine optimal therapies to minimize recurrence.

References:
1. O'Connor KC, McLaughlin KA, De Jager PL, et al. Self-antigen tetramers discriminate between myelin autoantibodies to native or denatured protein. Nat Med. 2007 Feb;13(2):211-7.
2. Jurynczyk M, Messina S, Woodhall MR, et al. Clinical presentation and prognosis in MOG-antibody disease: a UK study. Brain. 2017 Dec 1;140(12):3128-3138.
3. Jarius S, Paul F, Aktas O, et al. MOG encephalomyelitis: international recommendations on diagnosis and antibody testing. J Neuroinflammation. 2018 May 3;15(1):134.
4. Hacohen Y, Wong YY, Lechner C, et al. Disease Course and Treatment Responses in Children With Relapsing Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease. JAMA Neurol. 2018 Apr 1;75(4):478-487.
5. Narayan R, Simpson A, Fritsche K, et al. MOG antibody disease: A review of MOG antibody seropositive neuromyelitis optica spectrum disorder. Mult Scler Relat Disord. 2018 Oct;25:66-72.
6. Sechi E, Cacciaguerra L, Chen JJ, et al. Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD): A Review of Clinical and MRI Features, Diagnosis, and Management. Front Neurol. 2022 Jun 17;13:885218

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