DIFFERENT PATHOGENESIS OF THALIDOMIDE NEUROPATHY IN MULTIPLE MYELOMA.

Abstract

Background: In the past few years thalidomide became one of the most interesting chemotherapeutic drugs in the treatment of multiple myeloma. However a predominantly sensory neuropathy is a well‐known side effect of thalidomide in a substantial amount of patients. Peripheral nerve damage resulted to be at lest partially reversible only in 50% of cases suggesting a possible toxic effect on dorsal rot ganglion neurons. Spinal cord MRI was indicated as a useful tool in the diagnosis of sensory ganglionopathy. We described MRI findings in 6 patients with thalidomide neuropathy and multiple myeloma. Patients: Six patients (4 men, 2 women, mean age 61.2 ± 8.6 years) were included: two had non‐secretory, 3 osteolytic and 1 osteosclerotic myeloma. Thalidomide was administered orally at a dose of 200 mg/day in 4 patients, and at a dose of 100 mg/day in 2. All patients where asymptomatic for peripheral neuropathy before treatment. Five of them were previously treated with vincristine and 4 with cisplatin, both at low doses. Positive sensory symptoms developed 6 to 19 months after treatment beginning: all patients had paresthesia; 2 had pain in stocking and glove distribution. One patient developed sensory ataxia. On nerve conduction studies, all patients had decreased or absent sensory action potential both at upper and lower limbs. Methods: Cervical spine routine MRI was performed in all patients with a 1 T system, with sagittal T2 FSE spin echo (TR/TE excitations 3909 / 112), axial gradient echo (630/22/30)—weighted images. Results: Cervical spine MRI was normal in 5 patients. In 1 patient, however, MRI disclosed a small T2‐weighted high signal intensity in the posterior columns. Discussion: Our results suggest that thalidomide could have a different toxic effect on the peripheral nervous system than on dorsal root ganglion neurons and axons.