We report a 35-year-old male who developed severe neurotoxicity during ABVD treatment for stage IIb HL. He tolerated chemotherapy until the 5th cycle, but then developed paresthesias in his feet. By the end of chemotherapy, he had developed profound symmetric, length-dependent sensory loss, reduced reflexes, and weakness in the lower extremities. Upper extremities were spared. EMG showed severe polyneuropathy with features suggesting both demyelinating and axonal process without conduction block or temporal dispersion. Extended genetic testing showed no known mutation. Lumbar puncture was normal except elevated CSF protein of 91mg/dl. Trial of IVIG offered no improvement. Over the following 6 months, he developed hyperreflexia in the upper extremities and knees. Ankle reflexes remained absent with mute plantar responses. Brain MRI revealed symmetric T2 hyperintensities involving bilateral cortical spinal tracts consistent with a neurotoxic process. C-spine MRI was negative for cord lesion. Labs including hemoglobin A1C, B12, SPEP were normal.