We studied the effect of lidocaine on nerve conduction in vivo. Recovery of the compound muscle action potential (CMAP), sensory nerve action potential (SNAP), and single motor unit potential (MUP) of median nerve stimulation was recorded in four healthy volunteers after intravenous infusion of 20 ml of 0.5% lidocaine. During loading, CMAP and SNAP amplitudes rapidly decreased and their latencies increased. After recovery of the CMAP and SNAP amplitudes, nerve conduction velocity improved gradually over a period of 3-6 h, the amplitudes and configurations of CMAP and SNAP remaining unchanged. The conduction velocity of the single MUP markedly slowed before it is blocked. This indicates that maximum conduction velocity of CMAP and SNAP could be slowed by the partial inactivation of sodium channels without accompanying conduction block. Prolongation of the rise time of depolarization of the axonal membrane potential may be the active mechanism in this slowing because of sodium channel inactivation. Abnormalities in sodium channels at the nodes of Ranvier should be considered as a mechanism of conduction slowing even when there is no conduction block.