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J Neurophysiol 86: 402-411, 2001;
0022-3077/01 $5.00
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The Journal of Neurophysiology Vol. 86 No. 1 July 2001, pp. 402-411
Copyright ©2001 by the American Physiological Society

Cortical Representation of the Sensory Dimension of Pain

Robert K. Hofbauer,1,2 Pierre Rainville,3,4 Gary H. Duncan,1,2,4,5 and M. Catherine Bushnell1,2,5,6

 1Department of Neurology and Neurosurgery, McGill University; and  2McConnell Brain Imaging Center, Montreal Neurological Institute, Montreal, Quebec H3A 2B4, Canada;  3Division of Behavioral Neurology and Cognitive Neuroscience, Department of Neurology, University of Iowa Hospitals and Clinics, Iowa City, Iowa 52242;  4Département de stomatologie, Faculté de médecine dentaire and  5Centre de recherche en sciences neurologiques, Université de Montréal, Montreal, Quebec H3C 3J7; and  6Department of Anesthesiology, McGill University, Montreal, Quebec H3A 1A1, Canada

Hofbauer, Robert K., Pierre Rainville, Gary H. Duncan, and M. Catherine Bushnell. Cortical Representation of the Sensory Dimension of Pain. J. Neurophysiol. 86: 402-411, 2001. 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.




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