Anatomical localization and intra-subject reproducibility of laser evoked potential source in cingulate cortex, using a realistic head model.

OBJECTIVES: To (i) accurately localize the cingulate source of late laser evoked potentials (LEPs) using a realistic head model incorporating the individual's anatomy and (ii) assess the within-subject reproducibility of this source. METHODS: Late LEPs, elicited by painful CO2 laser stimulation of the right forearm, were recorded from 62 electrodes in one healthy subject. This was repeated 9 times, over 3 different days. Dipole source localization (CURRY 4.0) was performed on the most prominent (P2) peak of each LEP data set, using a head model derived from the subject's structural magnetic resonance image. RESULTS: In all cases the P2 LEP peak was best explained by a dipole located close to the border of the caudal division of left anterior cingulate cortex with left posterior cingulate cortex (mean residual variance was 1.7+/-0.4%). The maximum standard deviation from the mean dipole location was 3.2 mm. CONCLUSIONS: This study demonstrates that the location of the cingulate source of late LEPs is highly reproducible within this subject, when analyzed in this way, and suggests involvement of caudal cingulate regions in pain processing.

Differential effects on the laser evoked potential of selectively attending to pain localisation versus pain unpleasantness.

OBJECTIVE: To determine the effects on the laser evoked potential (LEP) of selectively attending to affective (unpleasantness) versus sensory-discriminative (localisation) components of pain. METHODS: LEPs, elicited by painful CO2 laser stimulation of two areas of the right forearm, were recorded from 62 electrodes in 21 healthy volunteers, during three tasks that were matched for generalised attention: Localisation (report stimulus location), Unpleasantness (report stimulus unpleasantness), Control (report pain detection). LEP components are named by polarity, latency, and electrode. RESULTS: N300-T7 peak amplitude was significantly greater during Localisation than Unpleasantness. The difference in N300-T7 amplitude between Localisation and Control approached significance, suggesting an increased amplitude in Localisation compared with Control, rather than a reduced amplitude in Unpleasantness. Peak amplitude, latency, and topography of N300-FCz, P450, P600-800 (early P3) and P800-1000 (late P3) did not differ significantly between tasks. CONCLUSIONS: These results suggest that the N300-T7 LEP peak reflects the activity of cerebral generators involved in the localisation of pain. The topography of N300-T7 is consistent with a source in contralateral secondary somatosensory cortex/insula and maybe primary somatosensory cortex. SIGNIFICANCE: This study confirms a role of the lateral pain system in the localisation of pain, and distinguishes it from stimulus novelty or attention.

Source localisation of 62-electrode human laser pain evoked potential data using a realistic head model.

Laser evoked potentials (LEPs), elicited by painful laser stimulation of the right forearm, were recorded from 62 electrodes in a single healthy subject. The positions of the electrodes on the scalp were co-registered with the subject's structural magnetic resonance image (MRI) of the brain. Spatio-temporal dipole modelling, using a head model derived from the MRI, estimated sources in left posterior cingulate, posterior parietal and anterior insular cortices. The parietal source peaked in activity at 260 ms, which explained the N1/N2 peaks of the LEPs. The cingulate source was the most strongly activated, at 400 ms, and accounted for the P2 LEP component. The insular source showed late, prolonged activation, peaking in magnitude at 850 ms. This is the first study to report scalp-recorded LEP generators in posterior parietal and insular cortices. Although these sources require replication, they are consistent with other functional imaging studies.