Peripheral Nervous System Manifestations of MOG Antibody Associated Disease
Pranjal Gupta1, Pritikanta Paul3, Vyanka Redenbaugh2, Yong Guo2, Claudia Lucchinetti4, Yahya Abdulrahman2, Abhigyan Datta2, Shailee Shah5, Christopher Klein2, Sean Pittock6, Eoin Flanagan2, Divyanshu Dubey2
1Neurology, Mayo Clinic, 2Mayo Clinic, 3University of Illinois at Chicago, 4University of De Medical School, Health Learning Blg, 5Vanderbilt Multiple Sclerosis Center, 6Mayo Clinic Dept of Neuro
Objective:

To determine the pattern of peripheral nervous system involvement in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD).

Background:

Recent studies have reported peripheral neuropathies in patients harboring myelin oligodendrocyte glycoprotein (MOG) antibodies but often lacked testing of disease controls.

Design/Methods:

It was a retrospective cohort study carried out at Mayo Clinic (Minnesota, Florida, and Arizona). Patients consecutively tested for MOG-IgG1 (January 1, 2003, to June 30, 2021) were included. Healthy human controls’ spinal cord, root and dorsal root ganglion were examined for MOG expression. All MOG-IgG1 seropositive patients were divided into three groups a) MOGAD with PNS involvement b) MOGAD with an alternate etiology of PNS involvement c) MOG-IgG1 false positive cases with PNS involvement. Archived sera from well characterized neuropathy/neuronopathy patients (n=196) were also evaluated for MOG-IgG1.

Results:

From a total of 279 patients , 215 fulfilled the international MOGAD diagnostic criteria. 15 of them were found to have PNS involvement. Six (median titer 1:40 (range 1:20 -1:100)) out of  215 MOGAD patients had PNS involvement that occurred concurrently with CNS demyelinating episode. Polyradiculopathy (6/6) was the most common phenotype of PNS disease. MRI of all six patients showed enhancement of the cauda equina nerve roots. Nine (median titer 1:500 (range 1:20-1:1000)) patients with true positive MOG-IgG1 had PNS involvement that was temporally unrelated to a CNS demyelinating event. All these patients had an alternate etiology of PNS involvement. Additionally, five (median titer 1:20 ) out of 196 patients sera from well characterized neuropathy/neuronopathy with an alternative etiology tested positive for MOG-IgG1 (amyotrophic lateral sclerosis, n =3;  small fiber neuropathy, n =1; distal acquired demyelinating sensory neuropathy,  n =1).

Conclusions:
Peripheral neuropathy is not a feature of MOGAD but inflammatory nerve root involvement can occur concurrently with CNS demyelinating events.
10.1212/WNL.0000000000204362