Late Adult Onset Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease: Clinical Characterization and Predictors of Outcome
Alessandro Dinoto1, Laura Cacciaguerra1, Nisa Vorasoot1, Vyanka Redenbaugh1, Alfonso Lopez1, Cristina Valencia1, Kai Guo1, Smathorn Thakolwiboon1, Susan Horsman1, Stephanie Syc-Mazurek1, Nanthaya Tisavipat1, Deena Tajfirouz1, Eric Eggenberger1, Misha Pless1, Kevin Chodnicki1, Jan-Mendelt Tillema1, Sean Pittock1, John Chen1, Eoin Flanagan1
1Mayo Clinic
Objective:

To assess the frequency, characteristics and outcomes of late adult onset Myelin oligodendrocyte glycoprotein antibody-associated disease (LO-MOGAD) and compare to early adult onset (EO-MOGAD).

Background:

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) can occur at any age, but data regarding LO-MOGAD are scant.

Design/Methods:
Patients diagnosed with MOGAD per current diagnostic criteria with age at onset ≥50 years-old were included. Clinical, laboratory, radiological, treatment and outcome data were retrospectively collected. We compared: a) patients with age at onset 50-59 and ≥60 years-old; and b) LO-MOGAD ≥50 years-old to n=141 patients with EO-MOGAD (age range:18-49). Binary logistic regression was performed to find predictors of disability and relapsing course at last follow-up.
Results:

We included 107 patients, representing 25% of the patients in the Mayo Clinic MOGAD database (n=436). Median age at onset was 59 years-old (range: 50-88) and 71 (66%) were female. Medical comorbidities were noted in 86/105 (83%). Optic neuritis was the most frequent phenotype at onset (77/107, 72%); median Expanded Disability Status Scale (EDSS) at nadir was 3 (range:1-9). In 32/107 (30%) cases a potential trigger was noted, mostly infections. In 32 patients (30%) an alternative diagnosis was assigned, most commonly giant cell arteritis (n=15). By a median follow-up of 22 months (range: 0-306), 50 (47%) patients had a relapsing course, and preventive treatment was administered in 53 (50%). Medication side effects were common (41/107, 38%). Follow-up duration predicted relapses; EDSS at nadir predicted residual disability. No differences were observed in patients aged 50-59 versus ≥60 years. Compared to EO-MOGAD, LO-MOGAD had more optic nerve, brainstem/cerebellar involvement and cognitive decline (p<0.05) and less frequent myelitis (p<0.05). EDSS and relapsing disease course were similar.

Conclusions:

LO-MOGAD accounts for 1/4 of cases and optic neuritis is the dominant phenotype. In this age group, MOGAD is under-recognized and frequently misdiagnosed. Outcomes in LO-MOGAD and EO-MOGAD are comparable.

10.1212/WNL.0000000000211822
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