101. Thalidomide-related peripheral neurotoxicity: Not only a sensory axonal neuropathy

Abstract

To recognize different type of thalidomide-related neuropathy (TRN) reviewing electrophysiologic data. We evaluated the follow-up of nerve conductions studies of 58 children affected by immune-mediated pathologies who had received doses ranging from 25 to 100 mg/day of thalidomide. 40 of 58 patients (69%) developed the electrophysiological findings of axonal neuropathy: 31 (53%) had pure sensory and 7 (12%) had sensory-motor neuropathy, while 2 (3.4%) had motor axonal neuropathy. Sural sensory nerve action potential (SNAP) and peroneal compound muscle action potential (CMAP) amplitudes were more prominently reduced compared to SNAPs and CMAPs obtained from the upper extremities and CMAPs from tibial nerve. Peroneal CMAP amplitude at lower limit at baseline evaluation was found in patients who developed motor neuropathy. We recorded a trend to increased incidence of TRN if thalidomide cumulative dose was >20 g except for pure motor neuropathy. Timely dose reduction or withdrawal of thalidomide can lead to improvement electrophysiological data in up to one years; however, in some cases, neuropathy is irreversible. Our results suggest that thalidomide induces a length-dependent axonal neuropathy, dose dependent if sensory and not if purely motor. The patient must be studied before treatment and monitored closely to prevent irreversible consequences.