Adam Shriver


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Differences in the Intensity of Valenced Experience across Species

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. 

Differences in the Intensity of Valenced Experience across Species

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:

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: and see also: ).  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.

Differences in the Intensity of Valenced Experience across Species

Since you mention pain several times, one pretty significant gap in this discussion is consideration of the dissociation between the sensory and affective components of pain experience.  The reported intensity of pain is correlated with the reported unpleasantness of pain, but the two components can be pushed in opposite directions (for example, reported  pain intensity can remain constant while pain unpleasantness is increased or decreased).  The affective component of pain is presumably what matters morally, and valance is definitionally part of the affective component. 

This is important because a lot of your discussion of pain is referencing the reported sensory intensity of pain.  For example, the gamma band oscillations appear to be tracking the sensory component of pain (the Yue et al article traces it to the primary somatosensory cortex). This would suggest that even if these oscillations are relatively predictive of pain, they are not good candidates for biomarkers that could be used to tell us something about the moral status of other species, since they occur upstream of the neural activity connected to affect. 

Interview with Jon Mallatt about invertebrate consciousness

This is super interesting...thanks Max!

I haven't read the books so I assume they deal with this there, but what about cases of blindsight, where people self-report that they don't see objects in certain parts of their visual field but nevertheless are able to respond above chance on forced choice tasks and even make appropriate grasping motions for objects in that area of the visual field? Wouldn't those, if true, be cases where we have maps of our surrounding environment that guide behaviour but nevertheless are not phenomenally conscious?

Also, a couple of the things he said about pain seem incorrect to me. He says "I think consciousness can come in degrees, but not in a way related to the invertebrate-versus-vertebrate status. Rather, it relates to the number of sensory receptors possessed. For example,some people have few pain-sensing neurons and are insensitive to pain whereas other people with more pain neurons are more sensitive to pain." But in all the studies I've seen, individual differences in how sensitive people are to pain have to do with neurons *in the brain* not with how many nociceptors in the peripheral nervous system someone has. After all, if all of the information from the peripheral nervous system is funnelled through the spinal cord to specific tracts in the brain, what ultimately matters is the coded information coming from that tract. In other words, if a given spinal neuron passes on the information [50 actions potentials in time span X] to a particular brain region, it doesn't really matter whether that signal was caused by 1 nociceptor or 100 nociceptors.

Finally, he seems to fall into a inexplicably common mistake of assuming that the difference between "fast pain" (transmitted through A-delta fibres) and "slow pain" (via C fibres) maps onto the difference between sensory and affective pain. I'm not sure why that is such a common move, but it's not really pain can lead to pain affect and suffering. I guess since he says that fast pain can lead to "misery," this suggests that he's not ruling out all affect, but it seems like an odd definition of suffering to me to restrict it to slow pain.