Pain Intensities
Kim Soland
I’m honored to have my work selected for the Griffith award and grateful for the opportunity to share a summary of it here.
Pains are standardly conceived as featuring a variety of phenomenal qualities and a singular magnitude: pain intensity. But there are circumstances in which pain’s sensory intensity may be phenomenally distinguished from its affective intensity. For example, a study by Valentini et al. (2013) found that hypnotic suggestion may alter pain’s affective intensity independently of its sensory intensity. Accordingly, a theory of pain requires an account of each of these magnitudes.
What is pain’s sensory intensity? A first approximation is negative: it is a magnitude, but not of its unpleasantness. What remains? An intuitive answer is that pain’s sensory intensity is stimulus intensity, akin to the felt intensity of innocuous temperatures and pressures. On the face of it, this account is copacetic with a straightforward representational analysis of pain’s sensory intensity, viz., that it representsa magnitude of some stimulus feature – how hot it is, how much pressure it’s applying, etc. However, if pain’s sensory intensity tracks stimulus feature magnitudes, and if some those features are the same ones tracked by innocuous touch, then we should expect a smooth grading between innocuous and noxious sensations. Take heat, for example. The heat pain threshold is roughly 108º F, meaning that ordinarily a tactile stimulus below that temperature doesn’t result in a pain experience. If the sensory intensity of a heat pain at the threshold represents that the temperature of the stimulus is 108º, and if the sensory intensity of a sensation just below that threshold represents that the temperature of the stimulus is 106º, then the pain should only feel a little more intense than the innocuous heat stimulus, just as a 106º stimulus feels only a little more intense than a 104º one. But that’s not how things go. There’s a sheer rise in sensory intensity at the pain threshold that doesn’t reflect a sheer rise in any distal magnitude, and so it’s implausible that pain’s sensory intensity represents the intensity of the painful stimulus.
I think pain’s sensory intensity reflects the salience of an underlying neural representation of a nociceptive stimulus. By salience I mean the amount of attentional processing that this representation receives. How much these resources are tied up by this nociceptive representation is reflected in its conscious rendering. Call this the salience view. The salience view is consistent with what pain scientists have discovered about the relationship between pain and attention as well as with an ongoing shift in the way that neural processing of pain is conceived.
A glut of research supports the claim that pains not only have an unusual ability to command attention but are also enfeebled when attentional resources are seized from them. For example, Eccleston (1995) finds that significant chronic pain profoundly and deleteriously affects performance on cognitively demanding tasks, Buhle & Wager (2010) catalog a wide variety of studies demonstrating that distracting subjects by engaging them in an attention-demanding task reduces the intensity of their pains, and Legrain, Perchet, and García-Larrea (2009) show that neural processing of pain competes with pain-unrelated activity for attentional resources. The salience view accommodates these conclusions straightforwardly: pains are typically highly intense becausethey are highly salient, and pains are less intense when attention is directed elsewhere because this redirection pulls attentional resources from nociceptive representations, rendering them less salient.
Unlike, say, the visual cortex for vision, there isn’t a discrete region of the brain that processes nociceptive stimuli. That’s why, for some time now, the standard line on pain in the brain is that it is realized the “pain matrix,” a highly distributed network of brain structures that, when firing collectively, constitute what is often called the “neural signature for pain.” But this view has a significant defect. As Ianetti and Mouraux (2010) and Legrain et al. (2011) demonstrate, nociceptive stimulus-caused activations in the “pain matrix” are spatially indistinguishable from activations caused by innocuous stimuli; the so-called “pain matrix” isn’t pain-specific. Nonetheless, regions of this network activate during nociceptive stimulation to a degree commensurate with stimulus intensity, which is how it came to be associated with pain in the first place. Why should this be? Ianetti and Mouraux and Legrain and his colleagues come to the same conclusion: it’s not a pain matrix, but a salience network. The reason this network fires up the way it does during nociceptive stimulation is because, as we have seen, representations of nociceptive stimuli are highly salient. One of the principal drivers of salience estimation is contrast: all else being equal, there is more contrast in the encoding of a more intense stimulus than a less intense one, and so more intense nociceptive stimuli are more salient than less intense ones. The salience view builds on this theory: salience differences explain both the correlation between noxious stimulus intensity and pain’s sensory intensity and the significant difference between the felt intensity of pains and innocuous touches.
A detailed explanation of this view and its implications may be found in Soland (2026).
Works Cited
Buhle, J., & Wager, T. D. (2010). Performance-dependent inhibition of pain by an executive working memory task. Pain, 149(1), 19–26.
Eccleston, C. (1995). Chronic pain and distraction: An experimental investigation into the role of sustained and shifting attention in the processing of chronic persistent pain. Behaviour Research and Therapy, 33(4), 391–405.
Iannetti, G. D., & Mouraux, A. (2010). From the neuromatrix to the pain matrix (and back). Experimental Brain Research, 205(1), 1–12.
Legrain, V., Iannetti, G. D., Plaghki, L., & Mouraux, A. (2011). The pain matrix reloaded. Progress in Neurobiology, 93(1), 111–124.
Legrain, V., Perchet, C., & García-Larrea, L. (2009). Involuntary Orienting of Attention to Nociceptive Events: Neural and Behavioral Signatures. Journal of Neurophysiology, 102(4), 2423–2434.
Soland, K. (2026). Pain Intensities. Philosophy and Phenomenological Research.
Valentini, E., Betti, V., Hu, L., & Aglioti, S. M. (2013). Hypnotic modulation of pain perception and of brain activity triggered by nociceptive laser stimuli. Cortex, 49(2), 446–462.