Abstract Details

Title Central or Peripheral? A Case of Demyelinating Neuropathy in a Patient With MOGAD

Topic Neuromuscular and Clinical Neurophysiology (EMG)

Presentation(s) P2 - Poster Session 2 (11:45 AM-12:45 PM)

Poster/Presentation
Number 9-007

Objective NA

Background

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a central nervous system (CNS) disorder in which immune-mediated demyelination affects the optic nerves, brain, and spinal cord. Myelin oligodendrocyte glycoprotein (MOG) is expressed on the outermost part of the myelin sheath of oligodendrocytes, creating a highly immunogenic target for MOG-IgG antibody. MOG-IgG antibody was only recently discovered in 2007. Epidemiology data on this clinical entity is limited. MOGAD is characterized by CNS findings, e.g. optic neuritis, transverse myelitis, cerebral cortical encephalitis, and meningitis. We present a patient with MOGAD who presented with peripheral nervous system (PNS) symptoms.

Design/Methods NA

Results A 27-year-old male presented with optic neuritis. Workup was negative for genetic and infectious etiologies. Serum assay showed low-positive MOG-IgG titers, and patient was diagnosed with MOGAD. Patient’s vision fully recovered. He presented eight months afterwards with sudden-onset ascending numbness and weakness in the extremities. He denied a sensory level, bowel/bladder dysfunction, Lhermitte’s sign, Uhthoff phenomenon. Neurologic exam showed hyporeflexia. MRI-spine showed multifocal short-segment T2 hyperintense cord lesions, with postcontrast enhancement. CSF showed 0 oligoclonal bands, 40 protein, and lymphocytic predominance. Nerve conduction study (NCS) demonstrated sensorimotor polyneuropathy with demyelinating features. Patient was treated with steroids and IVIG for acute Inflammatory demyelinating polyneuropathy (AIDP) versus MOG relapse. Patient’s strength and sensation improved. Reflexes became normoactive. Monthly-pulse IVIG was started to minimize future MOGAD relapses. Patient initially improved but then complained of worsening weakness in the upper and lower extremities. Repeat NCS redemonstrated sensorimotor demyelinating polyneuropathy.

Conclusions MOGAD is a CNS oligodendrocytopathy. Myeloradiculitis has been described, but other PNS involvement in MOGAD is rare. We present a case of combined CNS and PNS demyelination in a patient with low-positive MOGAD titers. Further investigation is warranted into the intersection of MOGAD and AIDP, the relapse rate and disease progression in these patients, and optimal treatment options.

Authors/Disclosures
Ayesha Saad (Northwell Neurology) PRESENTER	Dr. Saad has nothing to disclose.
Kiril Kiprovski, MD (NYU-Langone Health)	Dr. Kiprovski has nothing to disclose.
Kimberly O'Neill, MD	Dr. O'Neill has nothing to disclose.

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