Micheal, the link between specific brain regions and encoding pain affect is pretty complicated and controversial, as mentioned in the original article. So I would first note that even if we don’t know exactly what specific brain regions are doing, there’s still a lot of evidence (including several lines of evidence cited in the Price article you mention) for a sensory/affective dissociation.
That said, the brain regions most commonly linked to the affective dimension of pain are the anterior cingulate cortex (with some controversy as to whether the relevant region should be referred to as part of the midcingulate rather than the ACC), and the insula cortex (possibly along with the neighboring parietal operculum). But there was also a really impressively thorough recent study by Corder et a that seemed to show that the basolateral amygdala plays a central role in the unpleasantness of pain: https://science.sciencemag.org/content/363/6424/276 .
One difficulty with all of these regions is that they’re involved in many different cognitive processes, so it’s hard to suss out exactly what role is being played in pain. Part of what was especially cool about the Corder study was that it drilled down to specific neural ensembles within the amgdala that really did seem to play a pain-specific role. Similarly, more fine-grained examinations of the cingulate have helped to clarify which regions are involved in pain vs other processes: https://www.sciencedirect.com/science/article/abs/pii/S0891061815300326 and see also: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5801068/ ). The most detailed argument for a central role of the insula in pain affect is Grahek’s book Feeling Pain and Being in Pain, which is a bit dated now, but there’s still a lot of emphasis on the insula as a key area for pain’s unpleasantness. In humans, there’s evidence that lesions to the cingulate and insula can selectively impair pain affect while preserving pain sensation, direct stimulation of the insula can cause expressions of pain, and deep brain stimulation on the cingulate has selectively lessened the affective component of chronic pain in early studies.
So I guess the tl/dr is that the regions most likely to play a central role in pain affect are the anterior midcingulate cortex (which is the region Price referred to as the posterior ACC), the posterior insula and parietal operculum, and (specific neuronal ensambles in) the basolateral amygdala, but there are also a lot of really big questions remaining.
Jason, thanks for the response! I’d definitely be interested in talking more some time...I’m a bit of a novice on this forum so let me know the best way to set something up.
As a first pass at your questions, my chapter The Unpleasantness of Pain for Humans and Other Animals gets at some of them.
I think for (1), it depends on how strongly you mean “comes apart.” If we just mean varying one dimension while the other stays constant, or varying one dimension more than the other, there are a huge number of instances where this occurs. If, however, you mean the stronger case of “coming apart” where one dimension is present while the other is completely absent, the evidence is a bit more controversial. Lesion studies like cingulotomies and pain asymbolia cases (resulting from insula lesions) are often cited as examples, but some argue that cingulotomies don’t produce true dissociations and the pain asymbolia cases are pretty rare and a bit strange in other ways. Morphine or other opioids are sometimes said to eliminate pain affect without eliminating pain sensation, but again there are scholars who disagree with that interpretation. There are also many other forms of studies (such as direct stimulation, transcranial magnetic stimulation, deep brain stimulation) that are able to produce differential effects for pain affect and pain sensation, but I don’t think any of them have resulted in complete dissociations.
Regarding (2), I argued in the above chapter that we need better research into the nonverbal effects of sensory-affective dissociation in humans. A lot of the research on the unpleasantness of pain in humans relies too much on verbal self-report, which makes it difficult to know how to map this dimension to other animals (conditioned place aversion is currently one of the ways of trying to test pain affect).
Finally, you also asked:: “If sensory intensity and affective intensity are correlated in humans, do you think it’s reasonable to assume that the components are correlated in other mammals?”
So the typical pain signal in humans might follow roughly this pattern: a noxious stimulus causes activity in nociceptors in the peripheral nervous system, which then send a signal to the spinal cord, which transmits information to the thalamus, which then passes the info on to sensory cortical regions and to affective regions (and there are some direct connections between the thalamus and affective regions). I think the magnitude at every step in that process is pretty strongly correlated with the ultimate affective intensity. But we wouldn’t want to say activity in nociceptors is a biomarker for valences experience despite the fact that it is strongly correlated with it, because we know of many instances where nociceptive activity can come apart from experienced pain. Granted, the connection between the sensory dimension of pain is more strongly correlated with experienced unpleasantness, but it seems like the same problem exists. So I guess I just tend to think that “X is a neurobiological marker of Y” requires something stronger than “X is highly correlated with/and or predictive of Y.”
To take one example of why this could matter, an expectation of pain can influence pain unpleasantness more than pain intensity ratings. So if you were using a marker that only predicted pain intensity, you could miss important details about the actual welfare implications of the pains. Many of the pains that occur in agricultural animals or laboratory animals presumably occur in situations where differential influences (such as that from anticipated pain, high anxiety, depression, etc) on the affective components of pain could be important.