Dipole Source Analysis of Laser-Evoked Subdural Potentials Recorded From Parasylvian Cortex in Humans

Abstract

The location of the human nociceptive area(s) near the Sylvian fissure is still controversial in spite of evidence from imaging and evoked potential studies that noxious heat stimuli activate somatosensory areas in that region. Some studies have suggested the secondary somatosensory cortex (SII) on the upper bank of the Sylvian fissure posterior to the central sulcus, others the anterior insula or parietal area 7b. In this study, we applied dipole source analysis techniques to laser-evoked potentials (LEPs) that were recorded from subdural grid electrodes in three patients. As a functional marker, auditory-evoked potentials (AEPs) with a generator on the opposite bank of the Sylvian fissure were recorded from the same electrodes. The LEP global field power (GFP), a measure of spatial variance, showed a first peak at about 150 ms latency, corresponding to the latency of the N1 recorded from the scalp. In contrast to scalp recordings, the amplitude of the first GFP peak recorded from the grid was larger than the second peak (P2). This finding suggests that the generator of N1, but not that of later LEP components, was close to the subdural grids. When a regional source was fitted to the first GFP peak, its location was within the frontoparietal operculum in all patients. On average, the LEP source was 13 mm anterior, 6 mm superior, and 2 mm medial of the AEP source. This relative location also suggests a source within the frontoparietal operculum overlying the insula. At the latency of the first GFP peak, source orientation pointed inward, suggesting a generator within the inner vertical surface of the operculum. Somatotopy was assessed in one patient and was consistent with that of the projection area of the presumed nociceptive thalamic nucleus posterior part of the ventromedial nucleus, but differed from that of SII. These findings suggest that the nociceptive area in human parasylvian cortex that is activated most rapidly by noxious heat pulses may be separate from the tactile SII area.