Psychophysical methods were used to investigate pain in human subjects elicited by controlled freezing of the skin using a novel vortex thermode. When cooling stimuli delivered with a small thermode (7 mm diameter) exceeded the normal cold pain threshold into the sub-zero temperature range (-5 to -11 degrees C), all subjects reported an intense, sharp stinging pain sensation which occurred suddenly and was readily differentiated from normal cold pain. The onset of this stinging 'freezing' pain was closely correlated with a sudden increase in skin temperature beneath the thermode of 4.77+/-0.86 degrees C (+/-SD) associated with the phase transition of supercooled water to ice. The mean intensity of freezing pain was rated as 1.7 times as intense as cold pain at threshold. Subjects' mean reaction-time latency to signal stinging pain following the onset of phase transition on the volar forearm was 687+/-220 ms, which was slower than that for mechanically evoked impact pain. Freezing pain is suggested to be mediated by A-delta fibers, based on estimates of conduction velocity and on the observation that the freezing pain took on a burning quality of slower onset during an A-fiber pressure block of nerve fibers. We also investigated changes in skin sensation following the freezing stimulus, and found that freezing led to (a) an immediate, significant decrease in the cold pain threshold (to higher temperatures), which recovered to baseline in < 16 min, (b) a concomitant change in the quality of cold pain from dull to burning, (c) a significant, parallel increase in the threshold for the perception of cooling (to lower temperatures) which frequently manifested as a complete loss of cold sensation, and (d) a mild heat pain hyperalgesia which was still present 24 h later. The changes in thermal sensitivity were not accompanied by consistent changes in mechanical sensitivity. These results indicate that a characteristic sharp, stinging pain is reliably evoked abruptly at the phase transition of supercooled skin water to ice The ensuing brief decrease in cold pain threshold with burning quality, coupled with decreased sensitivity to cold, are speculated to reflect a central disinhibition of C-fiber nociceptor input due to reduced cold fiber activity. These effects may be relevant to frostbite, and distinguish themselves from the more pronounced thermal and mechanical hyperalgesia seen following intense freeze lesion of the skin.