Nerve conduction studies did not demonstrate abnormalities that specifically related to treatment with thalidomide. The motor nerve conduction data were all within the normal range for distal motor latency (peroneal, <5.8 milliseconds; tibial, <6.2 milliseconds; ulnar, <4.0 milliseconds; median, <4.2 milliseconds), for compound muscle action potential amplitudes (peroneal, >2.2 mV; tibial, >6.0 mV; ulnar, >4.0 mV; median, >6.0 mV), and for motor conduction velocities (peroneal, >40 m/s; tibial, >38 m/s; ulnar, >52 m/s; median, >50 m/s). Sensory nerve conduction was also within the normal range with the exception of 1 patient. This patient developed a decline and loss of the SNAP signals from her left sural and and left superficial peroneal nerves in association with clinical and imaging findings of a compressive left L5-S1 radiculopathy. Otherwise, the sensory nerve conduction data for the patients were within the normal ranges for the amplitudes of SNAPs (sural, >6 µV; superficial peroneal, >6 µV; ulnar, >17 µV; median, >20 µV) and for the sensory conduction velocities (sural, >40 m/s; superficial peroneal, >40 m/s; ulnar, >49 m/s; median, >48 m/s). Amplitudes of the SNAPs varied in the same nerve on different studies, but there was no consistent trend in the values to indicate a significant decline in amplitudes. Coexisting clinical conditions rather than the treatment with thalidomide caused neurologic symptoms.