Afferent fibers ending in nerve-end neuromas generate spontaneous impulse discharge which has been implicated as a cause of paraesthesias and pain following peripheral nerve injury in man. We now show in rats that the anticonvulsant drug phenytoin (PT), applied systemically or topically onto desheathed neuromas, suppresses the generation of neuroma discharge without blocking impulse conduction. The effect is dose-dependent and reversible upon drug washout. Since PT is known to provide effective pain relief in some kinds of neuralgia, the data suggest that the clinical analgesic action of PT in these conditions may, at least in part, involve a direct suppression of ectopic impulses generated in the region of the nerve damage.