Spinal Glioblastoma Mimicking Myelin Oligodendrocyte Glycoprotein Antibody Disease Transverse Myelitis
Objective:
To present a case of spinal glioblastoma mimicking myelin oligodendrocyte glycoprotein antibody disease (MOGAD).
Background:
Spinal cord lesions have a broad differential, with inflammatory, vascular, and malignant causes often misdiagnosed. MOGAD is an inflammatory disease responsive to immunosuppressant therapy, while malignancies require surgery, radiation, and chemotherapy. Positive antibody titers support the diagnosis of MOGAD, but false positive results have been reported at low titers. Studies on primary spinal glioblastoma are limited with no reported cases of positive MOG antibodies.
Results:
A 55-year old male presented with two months of leg weakness, paresthesias, and urinary retention. MR imaging showed longitudinally extensive abnormal cord signal from C3-C4 to T12 with 4.9x1.1cm rim-enhancing intramedullary lesion at T5-T6. MOG antibody titer was 1:40; other work up including cytology was negative. High dose steroids and three days of plasmapheresis (stopped due to allergic reaction) led to improved strength and cord edema regression, and the patient transitioned to a prednisone taper. Two weeks later, the patient developed arm weakness. Imaging showed progressive spinal cord edema. Additional history revealed symptoms developed a year before initially reported. Repeat testing was negative except unchanged MOG titer. After additional immunosuppressant therapy, imaging demonstrated unchanged enhancing spine lesion. Spinal biopsy revealed glioblastoma.
Conclusions:
Spinal cord malignancy can mimic MOGAD transverse myelitis. Chronicity and progression can aid in the diagnosis. This case highlights two atypical features for MOGAD: recurrence of cord signal changes and symptoms despite treatment, and the low elevation of MOG antibody titers, which raised suspicion for an alternative diagnosis. When atypical features are present in suspected inflammatory myelitis, a broad differential should be maintained. Studies show that patients with primary CNS malignancies can have signs of increased immune response, indicating that malignancy and autoimmune processes cause chronic immunologic dysfunction.