Well… It’s been a long while since I sat down and wrote anything more than a post for social media, text message, or clinical daily note. I’m not even sure if anyone reads blog articles anymore with the Instagram anatomy picture canned exercise craze and fitness model boomerang dances taking the world over.
But alas, I wanted to put some thoughts down in a deeper and more reflective format that 60 second videos and big text eye catching slides simply can’t capture. Read on if you’d like to follow along with or join into a discussion I’ve been having with myself.
I’m going to throw something out here, so read it with an open mind. I don’t know if the following text will be right, wrong, misguided, insightful, helpful, or just a big ole fat waste of time. I certainly don’t claim to know the matters covered in this article nearly as in depth as many of those people I silently follow along reading on social media long form discussions. My mind swirls with all of the information I am attempting to consume, refine, and build into a structured understanding of the best current evidence on the experience of pain. If I’m honest, I am writing this more as a method to try provide some of that ever-fleeting structure to the swirling storm of theories, terms, science, philosophy, and ponderings raging in my mind. I am open to your critiques and hope to learn more and struggle less by putting these thoughts down and out there to be ripped apart and sifted with a fine-toothed comb as I am so certain they will be.
My recent thoughts on pain:
Often it is stated that “nociception is neither sufficient nor necessary for the experience of pain” (this originated with Moseley I believe.) For ages I have taken this comment at face value, hung my hat on its validity, parroted it in lectures and conversations, and never really reflected on what it might mean or imply. Recently however, I have come to question just about everything in life ranging from this quote to the nature of reality itself (maybe too much booze and one too many philosophy podcasts). After much reflection and many discussions with myself, I am going to go out on a limb here and disagree to a certain extent with this quote. I know, disagreeing with the big man is probably not going to get me anywhere, but I think all ideas need to be challenged and discussing nuance is where progress is often made.
The above quote (given, we must recognize that it is taken out of context) states that nociception isn’t sufficient for pain. However, I think that I would like to argue that nociception is in fact sufficient for pain in many cases. Of course, not all pain all of the time is driven by nociception, and certainly what an individual experiences when they do have pain may diverge from the raw sensory nociceptive data in an infinite amount of ways based on associative learning, prior experiences, expectations, beliefs, context, other emotions, etc.). After reading this quote about 100 times now, I would like to make slight alterations to reduce the rate at which it is misconstrued and improperly parroted by many, including myself, who have been on the quest to learn more about pain. With a few small adjustments, I would like to rework that sentence to read “nociception doesn’t (always) directly cause pain and that pain can (sometimes) be felt in the absence of nociception.
Before we go any further and dive into where I think (I’m honestly not quite sure yet) I’m going with this, let’s take a step back by looking at what nociception is. According to the IASP:
“The neural process of encoding noxious stimuli” and that this process is conveyed by nociceptors which are “high-threshold sensory receptors of the peripheral somatosensory nervous system that are capable of transducing and encoding noxious stimuli”.
The IASP has gone through great care to make sure the definitions of nociception and pain are not conflated and that we as clinicians and researchers understand the difference between nociception and pain. Interestingly, if you look up the definition of noxious you find that noxious is described as a stimulus that is “harmful or injurious to health or physical well-being”. This leads me to believe that the definition of nociception should be changed to read “potentially noxious” stimuli as we know that nociceptors often depolarize and send action potentials up afferent pathways in the event of stimuli that are not harmful or injurious and in the event that the nociceptive ion channels have been sensitized by one of many mechanisms that may lead to the normal and most often beneficial phenomenon of peripheral sensitization. We are also quite aware that many people experience pain via the application of non-noxious (non-harmful or injurious) stimuli as a result of the well documented phenomena of hyperalgesia and allodynia. With this, the question arises of whether or not that experience of pain in hyperalgesia and allodynia is due to a human being that is interpreting incoming information as much more threatening or potentially harmful than they have in the past or other human beings would, or if that human being falls within normal ranges of “responsiveness” to ascending nociception and is simply responding with a greater pain experience as a result of significantly facilitated (maybe de-inhibited) ascending nociception…or of course, could it be both?
Now that we are all sufficiently confused about nociception, we can change gears and look closer at the experience of pain. If you are not familiar, the currently accepted (though hotly debated and potentially in need of updating) definition for pain is as follows:
“An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”
What I would like to focus on in this definition of pain is the SENSORY AND EMOTIONAL portion. This reading of the definition infers that ALL pain is both sensory and emotional all the time. Yet, I believe we may be able to look deeper and explore some scenarios in which this needs to be examined more deeply dissected apart.
I would like to argue (again, I recognize that I may very well be far off the mark) that pain can be, and sometimes is, a sensation in its own right before it becomes a sensory-emotional experience and that it is worthwhile to take time to discuss this idea.
Now before anyone gets up in arms, I AM NOT arguing in favor of a cartesian fallacy that pain is simply and only a sensory input. However, based on MY INTERPRETATION of the literature on neurophysiology and the pain experience, I would like to make the argument that pain can be a sensation, that pain can be an emotional experience, and that pain most often is a sensory-emotional experience that is emergent in nature.
To illustrate these concepts further, let’s look to some interesting examples and analogs:
A simple observation would be that this baby experienced pain in some capacity due to the physical response of withdrawal, yelping, crying, increased heart rate, increased respiratory rate, pupil dilation, etc. However, as we saw in the definition above, pain is a sensory AND emotional experience. With that in mind, we can arrive at the conclusion that for pain to be sensory and emotional it would be required that this newborn infant experienced emotion. No brainer right? On the surface level, this seems like a given and easy to agree with conclusion, but is it really that simple and straight forward? Interestingly, newer evidence from the lab of Lisa Feldman Barrett contradicts the historical concept of emotional fingerprints that are biologically inborn properties that are present from birth (or maybe even before). In place of these emotional fingerprints, Barrett proposes the theory of constructed emotion which would suggest that the experience of emotion is not yet possible until the baby has been exposed to culture, family dynamics, etc and had the ability to learn and develop the concept of emotions.
With fear of stepping on the toes of Steven Pinker, Barrett proposes that humans are somewhat of emotional “blank slates” that have dramatically different, genetically influenced, and biologically inbuilt affective drives. She proposes that we all “feel” this affect by way of the sensory information being transmitted to the brain for interpretation. This affect can be thought of being driven by interoception, or the sense of the internal state of the body, but importantly, it does not have a one to one relationship with the experience of emotion that will emerge from that human following the milieu of sensory information barraging the brain. Barrett would state that for emotion to truly exist, a person has to reflect on the biologically driven affect and pair that with the theoretically infinite number of priors that person may possess based on their unique history, family, culture, etc. Once this near instantaneous reflection occurs, an emotional experience unique to that person and molded by their specific genetically influenced affective responses and sociocultural concepts of emotion can then emerge. The totality of a living person is of course far more than their sensory information or their brain alone.
Before moving forward, let’s examine this concept of affect and constructed emotion on a deeper level. For example, lets take an example in which I am either tired, hungry, kicked, stabbed, sleepy, thirsty, or being cornered by a bear. We can see the role of affect through its influence on valence, arousal, and motivational intensity. In these scenarios, my interoceptive systems sense these changes in neuroimmune activity, autonomic, endocrine, and mesolimbic activity that are very much biologically driven. These sensations driven by changes in biologic activity cause me to feel a “pressure” to emote or act in some way. The change in neurotransmitters, hormones, and autonomic drive may sharpen or dampen my focus, influence my cognitive processing power, drive me towards aggressive tendencies, make me feel I need to propagate my genetic material, make me feel I need to enact a change to further my survival, stir a need to fight or flight, or any number of other rudimentary biologically driven responses.
However, it is of the utmost importance to emphasize that the experienced emotion that emerges following these internal stimuli will be unique to me and built upon the culture that I have grown up in, the family values and learned behaviors I have developed, the context of the situation in which the affective drives are being sensed, the norms my society has indoctrinated me with, the influence of my religion/faith if I happen to have one, and all of my past experiences. Theoretically, if another human, with a different prior than myself “felt” the same exact affect I did in any of those situations, they may have a completely different emotional experience emerge that is unique to them and their sociocultural norms and learned priors.
To take this one step deeper, the other human in the example who has unique priors, but “felt” the same exact affect as me may even generate an almost identical pattern of brain activity as measured by fMRI. Yet, this other human very well may report a completely different emotional experience. Despite our strikingly similar brain activity and biological drives, I may report a feeling of anger or frustration while this other human may describe a feeling of sadness or despair. Conversely, myself and the other human in this scenario may have different affects and fMRI red blob readings, yet report the same emotional experience.
This difference in reported emotional experience despite identical affect and fMRI findings or the same report in the face of diverging affect and MRI findings can be explained in some part by the phenomenon of “biological degeneracy”. Biological degeneracy can be described as the ability of elements that are structurally different to perform the same function/yield the same output, or the ability of elements that are structurally the same to perform a different function/yield a different output. Degeneracy may yield the same or different functions depending on the context in which it is expressed and is understood to be a prominent property of gene networks, neural networks, and evolution itself.
Now if we dig ourselves out of that rabbit hole and circle back to the previously mentioned example of the newborn baby responding to a noxious stimulus and reflect on what it is the baby is feeling, it would still appear they are likely feeling pain of some sort. That pain is very clearly driven by nociception, and based on the theory of constructed emotion is full of affect, but it very likely devoid of true emotion as we know it due to the fact that the baby has not yet been able to develop the concept of emotions through sociocultural learning. In this case it would appear that nociception is clearly sufficient for pain and that nothing other than sensory affect is necessary to lead to that experience. This could be thought of as a purely sensory discriminative sensation of pain.
Of course, for my hard noses out there, yes you could make the philosophical argument that we don’t know if this is pain or not because we cannot communicate with the baby. However, I think this is a weak argument based on the consistency and reproducibility with which all complex organisms respond to noxious stimuli.
It would appear to the astute onlooker that this dog has experienced pain. Yet, based on the IASP definition, pain is a sensory and emotional experience which dictates that this dog must have experienced emotion. Maybe anger at being poked? Maybe sadness at mistreatment? Maybe anxiety that it will be poked again?
But alas, the concept of animal emotion is one that stands on unstable ground and is hotly debated. If you again refer back to the work of Barrett, it would appear that we as human beings in all of our wonderful ability to fool ourselves may be committing the mental inference fallacy by projecting out concepts of emotions onto these furry friends of ours. To quote Barrett:
“Scientists automatically and unconsciously construct emotional meaning from the actions of their lab animals. That’s the mental inference fallacy. It happens every time scientists record a physical measurement and assign it a mental cause. “That growl is expressing anger.” “That change in heartbeat was caused by excitement.” “That brain activity was caused by disgust.” I’m not saying that animal actions are meaningless. I’m saying that it’s a scientific pitfall to presume that an action has emotional meaning.
In the world of animal research, mental inference is rampant. For example, baby rats, when separated from their mother after birth, make a high-pitched noise that sounds to us like crying. Some scientists inferred that the brain circuitry responsible for the crying must be the circuitry for distress. But these baby rats aren’t sad. They’re cold. The sound is just a byproduct as the baby rats try to regulate their body temperature — a task normally done by their absent mothers. It has nothing to do with emotion. But to an observer, even a well-meaning and highly intelligent one, the sound is easily and automatically perceived as sadness.
Mental inference is normal. Children assign fascinating personalities to their toys. Adults do likewise with their cars. People constantly guess at the meanings of each other’s actions, from raised eyebrows to teenage eye rolls. But scientists in the lab must resist the lure of mental inference, lest they fall prey to the mental inference fallacy and unknowingly taint their research.”
At this point, I feel it’s important to clarify that neither I nor Barrett necessarily believe or know with 100% certainty that animals do not experience emotion, but based on studies that attempt to control for the mental inference fallacy, it would appear that the answer is not as straight forward or clear as we have thought in the past.
I would argue, that this dog or the experimental lab rats do “feel” affect, or valence/arousal/motivational intensity. However, this affect again is primarily a biological drive influenced by the autonomic nervous system, endocrine system, and evolutionary pre-determined brain circuits that facilitate motivation to stay alive, safe, and well fed. This would not be the same as the higher-level complex experience of emotion as we commonly think of it.
Yet again, we could make the philosophical argument that we don’t know if this is pain or not because we cannot communicate with the dog. Again, I think this is a weak argument based on the consistency with which all complex organisms respond to noxious stimuli by displaying what is referred to as nocifensive behavior. Does this mean that the dog is experiencing pain just the same as you, me, or anyone else? Not necessarily at all. Though, it may imply and we may infer that, there is a rudimentary sensation of pain that is somewhat less complex and likely developed evolutionarily to better suit living organisms to survive and pass on their genetic material. Considering the universality of response to noxious stimuli with consistent “pain response behaviors” that are apparent in countless less complex organisms whom are unlikely to possess the capacity for emotion, it would seem unlikely we could make it to this point of existence without the experience of pain as a sensation. This indispensable pain sensation is hard wired into our nervous system, and has been essential for our survival to this point in time. As evolved as our higher level brain centers have become, we cannot fully escape the millions of years of evolution wired into our body systems that have been essential in threat detection, learning, and survival.
In the case of the LAD clogging, it clearly leads to tissue ischemia in the cardiac musculature, and that tissue ischemia leads to a drop in pH which leads to activation of nociceptive neurons which in turn convey information to your brain. You are a relatively healthy young person and have never had a heart attack in the past to “know what it feels like”, you were enjoying your day in a very non-threatening context, you had no reason to engage in any sort of emotional response in that instant (shortly after the experience of pain emotions can run high of course).
I want to focus at the very initial onset of pain in this scenario. Why in this case, would a person feel a sharp pain or deep cramping pain in their chest if not for nociception and nociception alone? There are no priors related to chest pain, no past experience of a heart attack, no imaging reports to prime one to be more reactive, no visual input to induce fear or misinterpret, no classical conditioning to explain away this pain as a learned response, no heightened stress levels and allostatic load to the system to blame, no catastrophic thoughts to conjure an emotionally mediated pain neurotag, and no emotion tied to this very initial experience of pain (in that immediate split second…within milliseconds later that can and certainly would change).
I think it is incredibly important here for me to make as clear as possible that I am trying to dissect this experience down as close to the initial onset of the “felt pain” as possible. It would be both foolish, and non-evidence based, for one to argue that after this pain arises to one’s conscious faculties it could or would not be heavily influenced, exacerbated, or maintained by the unique priors that hypothetical individual caries which would or course be heavily influenced by their experience with and knowledge of chest pain and heart attacks.
So, moving forward, the question that arises in my mind, is as follows:
“Was the very initial onset of pain that occurred completely out of the blue a sensory emotional experience, or was it simply the onset of pain as a sensation which resulted from nociception?”
I may be wrong (hopefully I’m stating this fact enough and readers recognize that I by no means have the strongest grasp on these concepts or claim to “understand pain”), but it does not seem unreasonable to me to theorize that pain may both be a sensation based on pure sensory-discriminative input at times, an emotion based on purely cognitive influences at others, and most often a sensory emotional experience. (more on this to come later)
Additionally, I hope it is clear that I am not making a claim that all pain is due to nociception or that nociception always causes pain. Examples of the absence of pain in severe tissue damage and/or high levels of nociception such as the soldier on the battlefield who is wounded but unaware, the gardener who has scratched their arm and only realizes after they see blood trickling down, and those who derive pleasure from BDSM (and have been shown to report less/no pain and present with brain scans that are starkly different from what would be expected when undergoing the sensory input they are) provide ample evidence that nociception does not equal pain. Additionally, examples of those who have experienced pain in the absence of tissue damage such as the famous story of the worker with a nail through his boot (but not his toe!), the rubber hand and fire and ice experiment, and reports of those who report a sudden pain experience simply by imaging an scenario they perceive to be dangerous or damaging all demonstrate that nociception may not be required at all for the experience of pain.
In this example, we can simply look to the analgesic effects of many medications to see a direct reduction in pain through simply removing ascending information tracking its way to the person’s brain. Without going deep into pharmacokinetics, NSAIDs are thought to work by inhibiting the activity of cyclooxygenase enzymes (COX-1 and/or COX-2). In cells, these enzymes are involved in the synthesis of key biological mediators, namely prostaglandins which are involved in inflammation which subsequently activates nociceptive neurons and transmission of nociception to the brain.
In a nutshell, opioid drugs, typified by morphine, produce their pharmacological actions, including analgesia, by acting on receptors located on both pre and post synaptic neuronal cell membranes. The presynaptic action of opioids to inhibit neurotransmitter release and the post synaptic action is often to reduce to likelihood of depolarization and continued transmission of action potentials up the spinothalamic tract. Additionally, it has been found that opioids also play a large role in activating descending modulatory effects from the periaqueductal grey matter which exerts its effects by inhibiting ascending information in the dorsal horn of the spinal cord.
Last but not least, we have corticosteroids which yet again function by decreasing inflammation.
“Chronic inflammation is characterized by the increased expression of multiple inflammatory genes that are regulated by proinflammatory transcription factors, such as nuclear factor-kappaB and activator protein-1, that bind to and activate coactivator molecules, which then acetylate core histones to switch on gene transcription. Corticosteroids suppress the multiple inflammatory genes that are activated in chronic inflammatory diseases, such as asthma, mainly by reversing histone acetylation of activated inflammatory genes through binding of liganded glucocorticoid receptors (GR) to coactivators and recruitment of histone deacetylase-2 (HDAC2) to the activated transcription complex.”
Each one of these medications have the capacity to decrease pain. Each one of the medications decrease pain by reducing the transmission of nociception to the brain through one mechanism or another. The fact that these medications work at all is evidence that nociception is in fact sufficient for pain in many cases and reducing nociception reduces the pain sensation which may in turn reduce the pain experience.
Considering all of the above mentioned scenarios, I’m going to go out on a limb here (it’s not really that far out on a limb and has been proposed by quite a few different people with quite a few different theories) and propose that pain might be something we can come to feel through a variety of different mechanisms. As alluded to earlier, it might be that in its simplest form, pain actually can be and is a sensation that arises to consciousness through the propagation of sensory-discriminative data reaching the person’s brain. In addition, it may be that pain can also be an emotion in and of itself based off of cognitive-affective status, as well as of course the commonly described combined sensory emotional experience that is mostly likely to describe the largest proportion of pain experiences.
Pain as a sensation (sensory-discriminative): Much of the first 3,000+ words of this article have been devoted to explaining and considering pain as simply a sensation. It seems strange to me that throughout all of human history pain has been viewed in this way, yet as our understanding of pain has expanded exponentially towards the impossible to arrive at asymptotic “truth” that is the human pain experience, I am now digging deep to find the words to describe it as such for fear of some “swinging” the proverbial pendulum too far to the philosophical and brain predictive side. Above we explored examples in which face validity seems to infer pain as a sensation. However, I wish to reiterate the point that I am not claiming this as truth by any means, but instead trying to make sense of research, reflect on real life examples, and create my own interpretations.
This idea of pain as a sensation driven by sensory-discriminative data begins to layer in complexity when we look to the overwhelming multitude of ways in which our peripheral and central nervous systems, immune system, and endocrine system may plastically change functionality to be better suited to convey nociception to the brain, thus increasing the likelihood of a felt sensation of pain.
The most commonly talked about phenomenon through which this occurs is of central sensitization. To quote Clifford Woolf (the man who discovered this phenomenon):
“A major feature of the nervous system is its plasticity or modifiability. The plasticity can be functional, reflecting altered activity due to changes in intrinsic excitability or synaptic transmission, chemical, due to altered expression or changes in the posttranslational state of proteins which modify the receptivity, activity or output of neurons, and structural, ranging from loss of neurons to establishment of novel connectivity. While such plasticity is often adaptive, enabling for example, learning and memory, it can be maladaptive, driving neuronal disease states. One prominent example of the latter are those forms of neuronal plasticity in nociceptive circuits in the central nervous system that constitute central sensitization and which represents a major underlying contributor to many persistent clinical pain states by amplifying pain.”
It is worth noting that the next to last word in this quote has been a point of much discussion. The “amplification” of pain is a descriptor that does not often sit well with those who dabble in the philosophy of pain, but in the hopes of not putting words into the mouth of a man much smarter than myself, I would venture to guess that Woolf here is referring to amplification of nociception which may in turn be an “amplifier” of the sensation of pain explored in the earlier parts of this article.
If we move away from the CNS, and look to the periphery we may also see the phenomenon of peripheral sensitization. Peripheral sensitization represents a reduction in the threshold and/or an increase in magnitude of responsiveness at the peripheral ends of sensory nerve fibers. This occurs in response to chemical mediators released by nociceptors and non-neuronal cells (e.g. mast cells, basophils, platelets, macrophages, neutrophils, endothelial cells, keratinocytes and fibroblasts) at the site of tissue injury or inflammation.
Another more contemporary concept that has been getting much air time in recent months is the phenomenon of neuroinflammation. This concept and associated research findings suggest that there may exist a degree of low-grade inflammation in the nervous system of many people that exerts consistent effects on that person’s nervous system which ultimately makes the depolarization of nociceptive neurons and subsequent transmission of nociception the brain much more likely to occur from what would normally be considered sub-threshold stimuli. To directly quote Ji et al.:
“Emerging evidence suggests that neuroinflammation contributes to the pathophysiology of co-prevalent or coexisting chronic pain conditions that are referred to as chronic overlapping pain conditions, which include but are not limited to fibromyalgia, headache, temporomandibular disorder, back pain, irritable bowel syndrome, primary headaches, pelvic pain, and vestibulodynia. Chronic overlapping pain conditions are characterized by symptoms consistent with the dysregulation of sensory, inflammatory, and psychologic domains.”
Peripheral sensitization, central sensitization, and increased neuroinflammation are all neuroimmune processes that increase pain through facilitation of nociceptive transmission. These are all examples of how our nervous systems and bodies are extraordinarily built to transfer nociception up to the brain and give strong biological plausibility to the possibility that pain, at least in its simplest form may be a sensation.
Pain as an emotion (cognitive-affective): Feeling the pain of losing a loved one. The pain of a rough break up and lost love. The pain of failure, disappointment, and sorrow. I don’t find it shocking at all human beings have come to the word pain to describe the aporia we feel from deep emotional trauma. From this alone, we may gain some insight into the emotional aspect of the human pain experience. Being in pain often mean to lose something; a movement, a function, an activity, a hobby, a job, a self, a life. Unsurprisingly, evidence has begun to demonstrate the close relationship between pain and emotion, most notably in cases of chronic pain. All experiences, especially vivid experiences such as pain and strong emotion can create lasting memories that exist as some unexplainable connection of synapses and neurotransmitter magic that exists within the person’s mind.
Interestingly, there appears to be evidence that as pain persists it transitions from “acute pain circuitry” to an experience that lays down neural roots in regions of the brain much more consistent with the experience of emotions. This is described as follows by Hashmi et al:
“In patients with acute and sub-acute back pain whose pain persisted over the observation period, persisting sub-acute back pain, we observed that the same percept of back pain, characterized by stable intensity and no discernable changes in anxiety or depression, is associated with a brain activity pattern that, in time, continuously shifts away from the meta-analytic acute pain circuit and progressively activates the emotion (as well as reward) circuit. Therefore, these longitudinal results replicate the cross-sectional between-subjects comparisons and reinforce that, even within the same individual, brain activity for back pain can activate different brain circuits.
It is remarkable that the brain signature for chronic back pain, once developed within the first year (as shown in persisting sub-acute back pain), is then stabilized and seems to remain constant over 10 years (brain activity for persisting sub-acute back pain at 1 year closely matches that for chronic back pain). Thus, within the first year, the brain carves a chronic pain state, implying that this first year can be viewed as a critical period for back pain chronification.”
This concept has become so strong that some have gone as far as to state that the “brain may be addicted to pain”:
“In accordance with these recent advances, we propose a novel definition of chronic pain. Rather than defining pain by its sensations, we propose a definition that emphasizes the neurobiological mechanisms that control behavioral adaptations, and we hypothesize that persistence of pain is likely mediated through the reorganization of the cortex by corticolimbic learning mechanisms. We therefore posit that chronic pain is a complex web of sensory and emotional experiences, coupled with behavioral adaptations. Specifically, we posit that the chronic pain state is a consequence of a change in value related to nociceptive afferent information impinging on the cortex, with limbic emotional learning mechanisms underlying this shift in value and with little opportunity to extinguish these emotional memories. Subconscious changes in contextual salience and the value of nociceptive inputs are signals that drive cortical reorganization, given that they render the pain more emotional and modify decision making and selection of behaviors. The net outcome is a brain that has learned to filter emotions, actions, and reward through the lens of pain, rendering the brain addicted to pain.”
I personally at this point have trouble wrapping my head around the concept of pain as an addiction. I should clarify that discussions with these researchers have actually yielded the concept of “relief from pain” as the addiction those with chronic pain are seeking and addicted to. This seems a little more palatable as addictions are primarily driven reward pathways and exemplified by compulsory reward seeking behavior. However, I am skeptical at this time to go so far as to hang my hat on the idea of chronic pain existing solely as an emotion or as a developed addiction based on brain imaging studies simply to the concept of biological degeneracy that was mentioned earlier. I think I would personally like to stick a pin in this and watch the evidence evolve over the next decade while considering that there is some biological plausibility based on brain imaging studies and addiction research but also the possibility chronic pain and addiction just happen to inhabit some of the same neural pathways and processes.
Pain as a sensory emotional experience: The sensory emotional experience of pain that emerges from a far more complex interplay between sensory information from the body that may be warped in untold ways through neuroplastic changes, learning, metabolic health, etc and that person’s own unique and infinity complex personal history, cultural and family learning, experiential learning, expectations, and immediate perception of their context. The sensory emotional experience of pain is not relegated to just the simple afferent input from a person’s periphery, their affect, their emotional status, or their priors. This is the experience of pain that comes to the minds of those of us who rack our brains trying to better understand the immense, murky, and mysterious quagmire that is “pain science”.
Of course, this again all becomes infinitely more complex when we start to layer on changes discussed earlier to the sensory system with repeated exposure to stimuli, metabolic dysregulation, injury, chronic low grade inflammation, sleep deprivation, differences in the sensory system from person to person as determined by genetic influence, nutrition, learning from culture, learning from family, learning from experience, learning from false information, influence of context on expectations, and all of the other ways in which we haven’t even learned yet that the sensory and perceptual systems can be altered and changed by environment, learning, and neuroplasticity.
I believe the sensory emotional pain experience is likely that which most of us feel most of the time when we have our own unique experiences of pain. We may “feel” sensory-discriminative inputs and the drives of affect, but these are most often woven into a very specific and infinitely complex context that influences what we come to experience and may not necessarily have a strong relationship with whatever it is that objective reality may be.
The preceding discussion of the infinitely complex dynamic between bottoms up and top down influences on the experience of pain ultimately leads to the theoretical concept of predictive processing as a means to better understand the concepts of consciousness and pain. Predictive processing is a framework involving a general computational principle which can be applied to describe perception, action, cognition, and their relationships in a single, conceptually unified manner. It is important to distinguish that predictive processing is not directly a theory about the underlying neural processes (it is computational, not neurophysiological), but there are more or less specific proposals of how predictive processing can be implemented by the brain.
Classical theories of sensory processing view the brain as a passive, stimulus-driven device. By contrast, more recent approaches such as the theory of predictive processing emphasize the constructive nature of perception, viewing it as an active and highly selective process. Indeed, there is ample evidence that the processing of stimuli is controlled by top-down influences that strongly shape the intrinsic dynamics of thalamocortical networks and constantly create predictions about forthcoming sensory events. (Engel et al).
Essentially, in a nutshell, the theory of predictive processing conveys the idea that the consciousness we experience, emotions we feel, and sense of self are all a hallucination generated by the brain based on assumptions of sensory information which are driven by priors and refined through error that is measured between the predictions and the actual sensory information we receive. The concepts of predictive processing are “sexy” to me, which immediately sends up a red flag that I need stay conscious of my biases. When trying to challenge my own affinity for this concept, I have come to the recognition that predictive processing appears to fall prey to the “ghost in the machine” philosophical error which perpetuates the concept of mind body duality. It has even been described by the hypothetical scenario below:
You are imprisoned in the control room of a giant robot. […] The robot inhabits a dangerous world, with many risks and opportunities. Its future lies in your hands, and so, of course, your own future as well depends on how successful you are in piloting your robot through the world. If it is destroyed, the electricity in this room will go out, there will be no more food in the fridge, and you will die. Good luck! (Dennett)
I fear that this approach will lose sight of the human being experiencing the pain and lead people to commit the mereological fallacy and neurocentrism that focuses all attention on the brain alone.
The Enactive Approach to Pain:
In an effort to confront the mind body dualism, ghost in the machine, and pain is in the brain concepts the enactive approach has been proposed in recent times. This reasoning can be described as follows by Stilwell and Harman:
“Pain is such a compelling topic, it incorporates human suffering and the importance of medical intervention. Many clinicians are still biomedically-focused, ascribing (intentionally or not) to early pain theories as they relay the message to patients that levels of nociception/tissue damage equal levels of pain. In contrast, some clinicians purport to embrace contemporary pain theories considered to be under the biopsychosocial umbrella, such as the neuromatrix theory. Yet, problematic neurocentric explanations are given, such as: pain is an output of the brain; the brain decides if you are in pain; pain is in the brain etc. Strictly tissue-based pain approaches have been heavily challenged, yet few have questioned the growing popularity of brain-centric pain explanations. Telling patients that their pain is in their brain does not fairly or accurately represent our understanding of the creation of the meaning of pain; on the contrary, it has clearly negative consequences.”
Stilwell and Harman go on the describe 5 E’s of the enactive approach:
Embodied: “Embodiment means not just having, and acting through, some physical instantiation, but recognizing that the particular shape and nature of one’s physical, temporal and social immersion is what makes meaningful experience possible.”
Embedded: “By virtue of being embodied, people are also automatically embedded or situated in an
environment, and perceptual changes can be viewed in relation to potential for action, based on what the environment affords.”
Enacted: “the idea that cognition is a relational process that is enacted (brought forth) through an organism’s embodied interaction with the world.”
Emotive: “the conceptualization that meaning (along with pain) is not a purely internal process; it is enactive-emotive where verbal suggestion, visual cues, and other contextual factors combine with past experience, knowledge, and attention/expectations to form meaning.”
Extended: “describes how enactivist approaches are like the concept of the extended mind in that cognition is not entirely Bin the head, but instead; it is distributed across the brain-body-environment.”
Stilwell and Harman go on to state:
“Considering the limitations of the pain theories presented, an enactive approach to pain was explored as an alternative big picture framework. Informed by established theory and research by phenomenologists and cognitive scientists, pain was described as: (1) Embodied, (2) Embedded, (3) Enacted, (4) Emotive, and (5) Extended. Overall, with an enactive approach, pain does not reside in a mysterious immaterial mind, nor is it entirely to be found in the blood, brain, or other bodily tissues. Instead, it is a relational and emergent process of sense-making through a lived body that is inseparable from the world that we shape and that shapes us. With this perspective the experience of pain cannot be observed or measured, and qualitative pain narrative remains the best available proxy for inferring pain in others.”
To say that pain is complex is an understatement and even a bit cliché. However, to postulate that we know even a fraction of what there is to know about the experience of pain lacks humility and falls starkly into the realms of Dunning and Kreuger. I recognize that this piece was long and a bit rambly, so if you have made it this far, I commend you…or you must have been pretty bored. This article reflects the lack of understanding I have and how disjointed my thoughts are on the topic and the sole purpose was to try and align my thoughts. I’m not sure that I’ve created more or less understanding and clarity for myself. However, with all of this reflection, I feel that it might be reasonable to theorize that pain may come to be through various mechanisms for different people at different times in different scenarios. It may be sensory-discriminative, emotional, and of course sensory emotional. It may be a sensation in some isolated cases, and it may be an emotional experience in others. We simply don’t know.
I have also recognized that we have several models through which we try to conceptualize pain. Some of these models “work” in some scenarios while falling short in others. It might be that we need a grand unifying theory for pain much like we are still in search of a grand unifying theory for how the universe works in theoretical physics. How far are we from achieving this? No one knows. Will there be yet another chasm to cross and intellectual hoop to jump through once we get there should that ever happen? Most certainly. So what lies next? I have no idea.
Thank you for reading,