Bilateral extensive corticospinal tract lesions in MOG antibody-associated disease.

A healthy 53-year-old man developed acute flaccid paraplegia, spinal sensory level, and urinary retention. Examination revealed bilateral pronator drift. MRI demonstrated demyelinating non-enhancing lesions involving corticospinal tracts (CSTs), middle cerebellar peduncles, and spinal cord (figure 1). CSF analysis disclosed lymphocytic pleocytosis and mildly elevated protein. Euroimmun fixed cell-based assay for serum anti–myelin oligodendrocyte glycoprotein (MOG) and anti–aquaporin-4 (AQP4) antibodies showed low positivity for MOG immunoglobulin G (IgG) (1:10). Treatment with high-dose glucocorticoids and IV immunoglobulin was effective (figure 2). Long CST lesions were found in anti–AQP4 IgG–seropositive neuromyelitis optica spectrum disorders.1 Bilateral extensive lesions following CST are a novel finding in MOG-related CNS autoimmunity.2