1116 - Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disorder (MOGAD) & The "H-sign": A Case Report

Thursday, February 19, 2026

5:00 PM - 6:30 PM AST

Presenting Author(s)

SM

Symonne Martin, MD

Resident Physician
Baylor College of Medicine
Houston, Texas, United States

Co-Author(s)

BG

Bernardo Gonzalez, MD

Resident Physician
Baylor College of Medicine
Houston, Texas, United States
JD

James Q. Doan, MD

Assistant Professor
Baylor College of Medicine
Bellaire, Texas, United States

Submitter(s)

sM

symonne Martin, MD

Baylor College of Medicine
Houston, Texas, United States

Case Diagnosis: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD)

Case Description: A 70-year-old male presented with acute right lower extremity weakness and numbness with progression to less than antigravity strength bilaterally. He also reported worsening constipation and urinary retention over the preceding 4-5 days. On admission, symptoms had partially improved, with exam findings consistent with T6 AIS D incomplete paraplegia and a particularly flat affect. Spinal MRI revealed an expansile T2 hyperintensity from T4-T7 with focal enhancement at T5-T6 and an “H-sign” suggestive of MOGAD. Concomitant congenital-on-acquired cauda equina compression from L2-L5 due to severe canal stenosis was also identified. Notably, brain MRI showed no acute infarct. The patient received five days of IV methylprednisolone followed by five days of plasmapheresis. Although NMO and anti-MOG antibodies were negative, prior steroid initiation may have increased the risk of false negatives. Upon completion of therapy, he was transferred to the Spinal Cord Injury unit for inpatient rehabilitation.

Discussions: MOGAD is a rare autoimmune demyelinating disorder, with international diagnostic criteria proposed only within the past five years. Patients commonly present with optic neuritis, transverse myelitis, or acute disseminated encephalomyelitis (ADEM), particularly in children. In MOGAD myelitis, the “H-sign” describes the involvement of spinal cord grey matter on axial T2 sequences with hyperintensity outlining the anterior and posterior horns, resembling an “H”. Studies estimate it is present in 30-60% of cases, and recognition may expedite diagnosis. Although there are no randomized controlled trials currently guiding treatment, evidence supports the role of high-dose steroids and plasmapheresis for acute attacks and relapse reduction. In this case, the patient had significant improvements on MRI following IV methylprenisolone/PLEX, further supporting the effectiveness of immunotherapy in suspected MOGAD.

Conclusions:
While additional research is needed on triggers, presentations, and treatment, this case highlights the value of radiographic evaluation and early immunotherapy when MOGAD is suspected.