Relapsing-remitting multiple sclerosis as a potential consequence of thalidomide treatment: A case report

We present the first reported case of central nervous system (CNS) demyelination associated with thalidomide. A 29-year-old female with a history of prurigo nodularis was prescribed thalidomide after the failure of other therapies. Three weeks later, she developed right hemiparesis and sensory disturbances in the right upper and lower extremities. Brain and spinal cord MRI showed hyperintense and gadolinium enhanced lesions. She was diagnosed with clinically isolated syndrome and treated with IV pulses of methylprednisolone with full recovery. Due to suspected association between her symptoms and thalidomide, the drug was discontinued. Three years later she returned to our Outpatient Clinic after being treated at another hospital for a new attack, characterized by muscle weakness and sensory disturbance in the lower limbs. Brain and spinal cord MRI showed new lesions, fulfilling the criteria for multiple sclerosis. We believe the association between thalidomide and CNS demyelination may be due to its tumor necrosis factor-α (TNF-α) inhibition effect. Biologic TNF-α inhibitors have been reported to cause CNS lesions, with cases of optic neuritis, transverse myelitis, multiple sclerosis, and neuromyelitis optica spectrum disorder developing after initiation of drugs such as etanercept, adalimumab, infliximab and golimumab. This report shows that thalidomide should be considered a potential cause of CNS demyelination, similar to biologic TNF-α inhibitors, and should be avoided in patients with a heightened risk.