Many ethicists writing about well-being have assumed that claims made about the relationship between pleasure and well-being carry similar implications for the relationship between pain and well-being. I argue that the current neuroscience of pleasure and pain does not support this assumption. In particular, I argue that the experiences of pleasure and pain are mediated by different cognitive systems, that they make different contributions to human behavior in general and to well-being in particular, and that they bear fundamentally different relationships to our motivational systems and hence desires. I further argue that though there is ample evidence that pleasure can be dissociated from appetitive motivation, there is no compelling evidence suggesting that the unpleasantness of pain can be dissociated from the aversive motivational force of pains. I consider several objections to this claim, including Jennifer Corns’ recent arguments that the unpleasantness of pain experience can be dissociated from the motivational signal of pain, before briefly drawing some lessons for ethics.
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We can further subdivide preference satisfaction accounts into actual preference views, which hold that well-being is improved by satisfying the preferences we have, and informed preference views, which hold that well-being is improved by satisfying the preferences we would have under some idealized conditions. This distinction will not be relevant for my discussion.
Some authors have suggested that pain asymbolia due to insula lesions represents the only “genuine” case of pain affect without sensory pain (Aydede 2005; Grahek 2001). I have argued against this view for a number of reasons. First, there is only very limited evidence reporting pain asymbolia and linking it to specific brain damage. Second, the reported symptoms of asymbolia suggest to me that something more is going on than just a loss of pain affect (Klein 2012 makes a related point about the stated symptoms of asymbolia). And finally, many of the claims suggesting that cingulotomy and morphine patients don’t have “true” dissociations are based on incorrectly assuming that their symptomology is the same as that of frontal lobotomy patients. I think the most parsimonious explanation is that the patients who report feeling pain but not being bothered by it in different conditions have something similar going on, though there are important differences between the various conditions.
There has been a relatively recent discovery of nerve fibers in mammals that appear to selectively respond to gentle touch such as massage (Vrontou et al. 2013). Knowledge thus far is limited. However, even if they exist and were a rough equivalent of “pleasure sensors,” pains and pleasures would still be relying on a different set of sensory transducers.
“Sufficient” as Berridge uses it, just seems to mean that, all other things being equal, causing neural activation in one of these regions in a healthy, normally functioning individual produces the effect (in this case pleasure or ‘liking’).
Berridge operationalizes “liking” by using it to refer to characteristic facial expressions rats make during presumably pleasurable experiences, facial expressions they share with humans and other monkeys. On Berridge’s view, liking isn’t necessarily conscious. For that matter, on his view, pleasure isn’t necessarily conscious. For the purposes of this article, when I use the term pleasure, I am referring to conscious likings. The possible existence of unconscious likings could be problematic for my account below if it turned out that the dissociation between wanting and liking only applied to unconscious likings, but the evidence doesn’t suggest this is the case.
I should note that the regions weren’t shown to be active during both pleasure and pain in the same experiments. Rather, Lecknes and Tracey were reviewing a number of different studies.
Donald Price, one of the pain researchers who has written the most about the affective and sensory pain pathways, has written that, “numerous studies support the view that the sensory and immediate affective dimensions of pain are separate and unique, even though they are closely related, (Price et al. 2006, p. 334). However, he also endorses a “serial pathway” model on which the sensory pain pathway serves as crucial input for affective processing, which integrates the sensory information with other relevant information (eg. the current level of anxiety). If the affective component of pain necessarily includes sensory information, one might question whether the two dimensions are truly dissociable. However, since the relevant question on my view is whether the motivational signal of pain dissociates from the feeling of unpleasantness, the possibility that the sensory component of pain contributes to the affective component would not undermine my core contention about the difference between pleasure and pain.
Of course, given that many areas in the brain do many things, it’s important to not make assumptions that two types of processes “are the same” or “involve a shared component” merely because they activate similar brain regions. However, I think what distinguishes this case is the level of precision involved: Wei and Zhuo (2006), for example, have tracked changes predictive of aversive motivation signals down to the level of cell layers in particular regions of the anterior cingulate.
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Shriver, A. The Asymmetrical Contributions of Pleasure and Pain to Subjective Well-Being. Rev.Phil.Psych. 5, 135–153 (2014). https://doi.org/10.1007/s13164-013-0171-2
- Negative Affect
- Anterior Cingulate Cortex
- Conditioned Place Preference
- Conditioned Place Aversion
- Sensory Transducer