A 49-year-old man presented to hospital with a 5-week history of progressive sensorimotor deficits affecting this ability to ambulate. He had mild COVID-19 infection four weeks prior to symptom onset. Examination revealed progressive weakness and hyperreflexia with severe sensory ataxia and T5 spinal sensory level. MRI brain and spine and extensive investigations for infectious, autoimmune, malignant, metabolic, and genetic causes were unremarkable. He received empiric immunotherapy for clinically suspected imaging-negative myelitis. Repeat MRI revealed linear,  increased T2 signal in the posterior limb of the internal capsule and midbrain and subtle symmetric longitudinally extensive increased T2 signal within the lateral columns extending from the craniocervical junction to the conus. He had clinical and radiologic improvement following plasmapheresis and maintenance intravenous immunoglobulin therapy.