This high-resolution electroencephalography (EEG) study tested the hypothesis that the suppression of rolandic alpha power before predictable painful stimulation affects the subject's subsequent evaluation of pain intensity, as a reflection of the influence of expectancy processes on painful stimulus processing. High-resolution EEG data were recorded (126 channels) from 10 healthy adult volunteers during the expectancy of a painful CO(2)-laser stimulation at the right wrist. Surface laplacian estimation enhanced the EEG spatial information content over 6 scalp regions of interest (left frontal, right frontal, left central, right central, left parietal, and right parietal areas). Spectral power was computed for 3 alpha sub-bands with reference to the individual alpha frequency peak (about 5-7 Hz for alpha 1, 7-9 Hz for alpha 2, and 9-11 Hz for alpha 3). The suppression of the alpha power before the painful stimulation [as reflected by the event-related desynchronization (ERD)] indexed the anticipatory cortical processes. Results showed maximum (negative) correlations between the alpha 2 and alpha 3 ERD amplitude at the left central area and the subjective evaluation of pain intensity (P < .001). The stronger the anticipatory alpha 2 and alpha 3 ERD, the higher the subjective evaluation of pain intensity. For alpha 3, that correlation was confirmed even when the effect of habituation across the recording session was taken into account. These results suggest that the anticipatory suppression of the alpha rhythms over the contralateral primary sensorimotor cortex predicts subsequent subjects' evaluation of pain intensity, in line with its crucial role for the discrimination of that intensity.
Perspective: This electroencephalographic study showed that anticipatory activation/deactivation of sensorimotor cortex roughly predicts subjective evaluation of pain. This motivates further investigation on possible implications for the understanding of central chronic pain. Chronic pain patients might exaggerate the anticipatory activation of sensorimotor cortex to negligible pain stimuli.