Cortical representation of the sensory dimension of pain.

By R. Hofbauer, Pierre Rainville, G. Duncan, M. Bushnell. Journal of Neurophysiology, 2001

603 citations recorded by the source corpus.

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.

Subfields: Clinical Psychology, Cognitive Neuroscience, Physiology

View Paper: https://www.semanticscholar.org/paper/27871ee6d21b5082bfe907118bf8c20ccbd7e17d

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Citations in the corpus

Pain and the brain: Specificity and plasticity of the brain in clinical chronic pain (2010, background): “Two elegant studies first established that human brain activity may be subdivided along emotional and sensory components [53,86], in whichmid-ACCwas identified as beingmodulated by affect andprimary somatosensory cortexby sensoryproperties of pain perception.”
Descending control of pain. (2002, background): “Evidence is accumulating that cortical structures fulfil a more active role in nociceptive processing than hitherto appreciated (Bolles and Fanselow, 1980; Burkey et al., 1996; Casey, 1999; Millan, 1999; Shi and Davis, 1999; Bechara et al., 2000; Fields, 2000; Price, 2000; Hofbauer et al., 2001; Joh”
Human brain mechanisms of pain perception and regulation in health and disease (2005, background): “A.V. Apkarian et al. / European Journal of Pain 9 (2005) 463–484 473 474 A.V. Apkarian et al. / European Journal of Pain 9 (2005) 463–484 involved depend on the nature of the suggestions (Rain- ville et al., 1997; Faymonville et al., 2000; Hofbauer et al., 2001).”
How do we perceive the pain of others? A window into the neural processes involved in empathy (2005, result): “The main finding of this study showing activation in the ACC and in the anterior insula during the perception and assessment of someone else’s pain is consistent with previous imaging studies of pain processing that have demonstrated their role in the affective aspect of pain processing (Coghill et ”
Exacerbation of Pain by Anxiety Is Associated with Activity in a Hippocampal Network (2001, background): “, the sensory dimension of thermal pain (Peyron et al., 1999; Hofbauer et al., 2001).”
Placebo Effects Mediated by Endogenous Opioid Activity on μ-Opioid Receptors (2005, background): “, 2000) and by more specific aspects of the pain experience, such as the pain intensity (Coghill et al., 1999; Hofbauer et al., 2001), its affective qualities (Rainville et al.”
The influence of negative emotions on pain: Behavioral effects and neural mechanisms (2009, positive): “Whereas hypnotic suggestions changing the sensory, but not the affective dimension lead to signal changes in the primary somatosensory cortex (Hofbauer et al., 2001), affective without sensory changes were correlated with activation in the anterior cingulate cortex (Rainville et al.”