Dowman R
Department of Psychology, Clarkson University, Potsdam, NY 13699-5825, USA.
Psychophysiology. 1996 Jul;33(4):398-408. doi: 10.1111/j.1469-8986.1996.tb01065.x.
The amplitude of the late pain-related negative-positive peak complex, which we have labeled SP3 (134-150 ms) and SP6 (277-331 ms), respectively, increased with increasing interstimulus interval (ISI). This contrasts with the nociceptive spinal withdrawal reflex and subjective pain rating data, which implied that nociceptive somatosensory processes were unaffected by ISI at stimulus levels that were well within the pain range. A scalp topographic analysis strongly suggested that none of the brain areas responsible for SP3 or SP6 are involved exclusively in nociception. We also observed a pain-related positive potential approximately 161-177 ms following sural nerve stimulation that has not been reported by others. A dipole source localization analysis and the effects of ISI and stimulus intensity on this potential suggest that it is generated by the response of primary somatosensory cortex neurons to inputs arising from the innocuous peripheral afferents and that this response is inhibited by noxious inputs.
