Pain as a homeostatic … emotion? (Member Post)

What are homeostatic “emotions”?

This is not about “emotion” in the familiar sense. Although it is meaningfully related.

The word “emotion” almost kept me from diving into this topic, so let’s start by clearing something up: it does not mean that pain is in the same class as feeling sad or mad or Weltschmerz (“world pain,” which I am feeling an awful lot of lately).

“Homeostatic emotion” is a technical term for feelings that tell us our physiological status: thirsty, tired, sick, hot, hungry, and so on. These have also been called “primordial feelings” and “homeostatic feelings,” and Dr. Bud Craig is the one who replaced “feelings” with “emotions.” I’m not sure if that was a good choice, but it’s what he went with, and he did not mean that feeling pain is like being in a bad mood.

Unless he did. Because part of the point here is that homeostatic emotions are cousins to feelings — but they are more fundamental and hind-brainy and (importantly) more motivating.

A new way to think about the nature of the pain beast

Craig proposed that pain evolved as part of the system that feels and reacts to internal physiological conditions to maintain homeostasis, making it “a specific emotion that reflects homeostatic behavioral drive, similar to temperature, itch, hunger and thirst.” (This all meshes quite nicely with my recent post about the evolutionary perspective on pain.)

This is in contrast to the more conventional view of pain being mainly about “the exteroceptive sense of touch,” a subcategory of touch. Ouchy touch.

Another way to put it: pain is not about sensing and interpreting the outside world (“exteroception,” sensing the outer world), but rather how the inside of the body is getting on (interoception, sensing the inner world), and responding to that. Homeostatic signalling — internal sensations about physiological state, e.g. “too warm” — is “a feeling from the body that motivates behavior.” They push us to act, to move away from the heat, or towards the food.

Neural pathways and anatomical structures relevant to the integration of bodily signals and emotional awareness. There will not be a quiz. Source: Craig, Trends in Neurosciences, 2003.

Scientists had already known that “pain and temperature are processed together in the mammalian central nervous system,” but Craig added “their underlying commonality as aspects of homeostasis.” That is, pain is handled by the same neurological systems as all the other homeostatic feelings. Craig’s 2003 paper appears to have been his magnum opus where he laid all this out in detail.

The neuroscience behind the theory

Craig was a neuroanatomist, so he brought the hard science and his exotic wiring diagrams. He argued that this is not just a thought experiment, but “arises directly from functional anatomical findings in cat and monkey,” carefully contrasted with human neurology. He explored several specific and technical examples in the paper.

The most interesting example to me: primates have a unique forebrain region devoted to integration of interoceptive information, or homestatic emotions. In other animals, the signalling pathway for internal weather reports only gets as far as the brain stem. This strongly suggests that our experience of pain is more tied into our complex minds, probably both affected by our psychology and also more capable of affecting it.

“Only primates seem to have the neuroanatomical capacity to feel pain in the same way that humans do.”

This surprisingly high-level processing of “primordial” feelings in humans is probably why he coined the term “homeostatic emotions.” He was saying that human pain gets a lot closer to being a part of our complex emotional reality than it does in animals. It’s probably no less motivating in animals, but for humans it also obviously gets more … well, emotional!

Another good example of an experimental basis for Craig’s hypothesis is that “cordotomy lesions interrupt these feelings”: that is, the same lesion that disrupts other homeostatic feelings (e.g. itch) also disrupts pain.

Meet the new boss, not the same as the old boss (and very technical)

Craig concludes by explaining in more detail how all of this contrasts with the “prior conventional view” (and still the conventional view now, despite his work). I’m also sharing this to give you a taste of how dense the paper is! Brace for impact…

It incorporates specific sensory channels for different kinds of pain and for pain of different tissue origins. It provides a fast (sharp) pain channel that can elicit fight-or-flight behavior and a slow (burning) pain channel that can engage long-term responses, sickness behavior and immune function. The discriminative, topographic representations in interoceptive cortex obviate the involvement of S1 in feelings from the body. Viewing pain as a homeostatic emotion readily incorporates the interactions of pain with other homeostatic functions and with emotional state, such as in psychosomatic illness. Sensitization of lamina I STT nociceptive neurons can easily explain neuropathic allodynia, and loss of the inhibition imposed on the motivational pathway by thermosensory activity provides a concrete anatomical model for central pain. This view also provides a clear explanation for the conjoint activation of the ACC and the right anterior insula in placebo analgesia.

Phew. I feel like it would probably take another few hundred words to translate that. But the gist is that this model can account for some aspects of pain that are tough to explain without it. Of the many that I could emphasize, I’d like to call out just one…

What does chronic pain “motivate”?

People have trouble with the idea of chronic pain as a “motivating” experience. We understand “pull hand away from hot stove,” but how are we supposed to react to stubborn pain with no clear cause? What is the “homeostatic emotion” of chronic pain motivating us to do about it? Craig is giving us the answer here: “sickness behaviour,” which means “hunker down, move less, be conservative, no adventures today.”

It’s a broad spectrum way of responding to “something” being wrong physiologically, and it is motivated by feeling lousy and fragile and sensitive (which is mediated by neuroinflammation). That pain-motivated behaviour has clear survival value in the big picture: generally doing less improves your odds of recovering from whatever is wrong. (If only it could guarantee it!)

I’ve written about sickness behaviour before, many years ago now. But Bud’s even older paper has definitely deepened my understanding of it.

I am not qualified to judge this paper strongly. I don’t know how effective Craig was at defending and supporting his idea. I do know that it seems impressive and fascinating from my perspective as a journalist.

It’s unclear to me how influential has been. According to ResearchGate, it’s been cited close to a thousand times, so clearly it has had some influence. But there was also very little follow-up work from Craig — this 2003 paper was his last major professional publication, I think.

UPDATE: He wrote a book! In 2015: How do you feel?

Unsurprisingly, Craig’s work has been interpreted — and likely over-interpreted — as “the background for our contemporary understanding of mind–body therapies” (Mehling, 2024). But treatments like meditation, yoga, and cognitive behavioural therapy have not — repeat, not — panned out as clearly effective. While Craig’s research sheds interesting light on the relationship between pain and psychology, that definitely doesn’t necessarily mean that the mind can relieve pain any more than it can stop you from feeling overheated or thirsty.