Cortical Representation of the Sensory Dimension of Pain

TLDR

Pain is a multidimensional experience, yet the neural representation of its dimensions remains poorly understood; prior work used similar techniques to modulate perceived unpleasantness of noxious stimuli. Ten volunteers underwent PET scans while receiving tonic warm and noxious heat to the hand under four conditions—alert control, hypnosis control, and hypnotic suggestions to increase or decrease pain intensity—to measure pain‑evoked cerebral activity. Noxious heat reliably activated contralateral S1, S2, ACC, and insula, and hypnotic modulation of pain intensity produced significant changes in S1 activity—unlike prior affect‑modulation studies that altered ACC—demonstrating a double dissociation that highlights sensory versus affective cortical specialization.

Abstract

It is well accepted that pain is a multidimensional experience, but little is known of how the brain represents these dimensions. We used positron emission tomography (PET) to indirectly measure pain-evoked cerebral activity before and after hypnotic suggestions were given to modulate the perceived intensity of a painful stimulus. These techniques were similar to those of a previous study in which we gave suggestions to modulate the perceived unpleasantness of a noxious stimulus. Ten volunteers were scanned while tonic warm and noxious heat stimuli were presented to the hand during four experimental conditions: alert control, hypnosis control, hypnotic suggestions for increased-pain intensity and hypnotic suggestions for decreased-pain intensity. As shown in previous brain imaging studies, noxious thermal stimuli presented during the alert and hypnosis-control conditions reliably activated contralateral structures, including primary somatosensory cortex (S1), secondary somatosensory cortex (S2), anterior cingulate cortex, and insular cortex. Hypnotic modulation of the intensity of the pain sensation led to significant changes in pain-evoked activity within S1 in contrast to our previous study in which specific modulation of pain unpleasantness (affect), independent of pain intensity, produced specific changes within the ACC. This double dissociation of cortical modulation indicates a relative specialization of the sensory and the classical limbic cortical areas in the processing of the sensory and affective dimensions of pain.