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.
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.
Great, this is fantastic, thanks! Clearly there is a lot more I need to think about! I just sent you a message to arrange a chat. For anyone following this exchange, I’ll try to post some more thoughts on this topic after Adam and I have talked.
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.
Great, this is fantastic, thanks! Clearly there is a lot more I need to think about! I just sent you a message to arrange a chat. For anyone following this exchange, I’ll try to post some more thoughts on this topic after Adam and I have talked.