The effects of a heterotopic cold pain stimulus applied to the hand on the scalp-recorded negative difference potential (NDP) and subjective pain ratings elicited by electrical stimulation of the sural nerve were examined in 24 participants. Our previous work strongly suggests that the NDP is generated in part by the cognitive division of the anterior cingulate cortex (ACCcd). The latency and magnitude of the ACCcd activity were estimated from the NDP and from the dipole source localization analysis of the NDP. As expected, the sural nerve pain ratings were smaller in the cold pain condition than in the control condition. The ACCcd activity underlying the 125-ms peak of the NDP did not change across conditions, whereas the ACCcd activity underlying the 210-ms NDP peak was largest in the cold pain condition. The dissociation between pain-evoked ACCcd activity and pain ratings observed here and elsewhere suggest that not all of the nociresponsive neurons in the ACCcd are involved in pain sensation. Rather, differences in the cognitive demands of the control and cold pain conditions suggest that the pain-evoked 210-ms ACCcd activity reflects response selection processes, perhaps response competition monitoring.

The effects of attentional set on subjective magnitude ratings, spinal reflexes, and somatosensory evoked potentials (SEP) elicited by innocuous and painful sural nerve stimulation were investigated in 24 subjects. Cuing stimuli informed subjects as to whether a visual identification or a somatosensory rating task would follow. Twenty percent of the trials were invalidly cued, where the subjects were expecting a visual stimulus but were given a sural nerve stimulus and vice versa. Subjective magnitude ratings were lower in the invalidly cued condition than the validly cued condition. Attentional set had no effect on innocuous-related spinal or early cortical responses, nor on the spinal nociceptive withdrawal reflex. The pain-related negative difference potential (NDP) and P2 component of the SEP were largest in the invalidly cued condition. These results provide further support for our hypothesis that the NDP is generated in part by the anterior cingulate, and suggest that the anterior cingulate response to pain reflects non-pain-specific cognitive processes (e.g., orienting attention towards important stimuli in the environment and/or response competition) and not some aspect of the pain experience. The effects of attentional set on the pain-related P2 suggests that it might correspond to the P3a event-related potential. If this is the case, the pain-related P2 could serve as a useful index of neural processes involved in the cognitive-evaluative aspect of pain.

Our recent work suggests that innocuous somatosensory activity elicited by a brief electrical stimulus is inhibited by pain evoked by the same electrical stimulus but not by pain evoked by continuous heat. These results led to the hypothesis, tested in the present experiment, namely that pain only inhibits innocuous somatosensation when the painful and innocuous stimuli have short durations and close temporal and spatial overlap. A painful 200-ms laser pulse did not produce a decrease in the perceived magnitude of the innocuous electrical stimulus or in the amplitude of a scalp potential that earlier work suggested is generated by neurons involved in innocuous somatosensation. Hence, the pain-related inhibition of innocuous somatosensation observed in these electrical studies cannot be attributed solely to the duration or to the temporal and spatial overlap of the innocuous and painful stimuli. Laser pain did produce a small increase in the subjective magnitude of the innocuous electrical stimulus, which the electrophysiological evidence suggests might be due to a change in the late- but not the midlatency responses in the central innocuous somatosensory pathways.