Clinical and electrophysiological evaluation of patients with thalidomide-induced neuropathy

Whether thalidomide induces a sensory ganglionopathy or a length-dependent axonal neuropathy is disputed. Moreover no agreement exists concerning the effects of thalidomide dosage on the clinical and electrophysiological findings.

We examined the effect of age, gender disease duration, total cumulative dose on the clinical and electrophysiologic parameters.

Fifteen patients who had previously received 100 mg/day of thalidomide for the treatment of multiple myeloma were evaluated retrospectively. Clinical findings and nerve conductions studies were evaluated using a modified total neuropathy scoring system.

Sensory symptoms (p = 0.033, r = 0.552) and objective sensory findings (p = 0.002, r = 0.730) worsened with higher thalidomide doses. There was no effect of age, gender and disease duration, neither on clinical symptoms and objective findings, nor on electrophysiologic data. Twelve patients (80%) developed the electrophysiological findings of neuropathy. Six (40%) had pure sensory and 4 (26.6%) had sensori-motor peripheral neuropathy, while 4 (26.6%) had carpal tunnel syndrome. Sural sensory nerve action potential (SNAP) amplitudes were more prominently reduced compared to SNAPs obtained from the upper extremities. Sural SNAP amplitude showed a tendency toward reduction as the total cumulative dose, although it is not statistically significant (respectively; p = 0.187). Significantly reduced ulnar peroneal and tibial compound muscle action potential amplitudes, slow motor nerve conduction velocities of the ulnar and peroneal nerves were found in the study group compared to reference norms (p < 0.05).

Our results suggest that thalidomide produces a dose dependent peripheral neuropathy, mainly localized to the peripheral nerves in a length dependent manner. The patient must be monitored closely to prevent irreversible consequences.