Is pain where you feel it in the body, or in the brain? Neurophenomenology and the spatial aspect of nociception

Pain is interesting, salient, mysterious. It may feel like it is in one specific place in or on the body. It may feel diffuse, with gradations, or it may seem referred from one area to another. What is happening in the brain and in the body as these spatial aspects of pain are experienced? How much of the causation of pain occurs where we feel it, and how much occurs in the brain? Below is a series of probes and thinking aloud about where pain is, with speculations to stimulate my thinking and yours.  I’m not a “pain expert”, nor a bodyworker that heals clients, nor a physiologist with a specialization in nociception, but a cognitive scientist, with clinical psychology training, interested in body phenomenology and the brain.  Please do post this essay to Facebook, share it, critique, respond, and comment (and it would be helpful to know if your background is in philosophy, neuroscience, bodywork, psychology, medicine, a student wanting to enter one of these or another field, etc). Pain should be looked at from multiple angles, with theoretical problems emphasized alongside clinical praxis, and with reductionistic accounts from neurophysiology juxtaposed against descriptions of the embodied phenomenology and existential structures.  As I have mentioned elsewhere, it is still early in the history of neurophenomenology…let a thousand flowers bloom when looking at pain. We need data, observations, insights and theories from both the experience side as well as the brain side. Francisco Varela aptly described how phenomenology and cognitive neuroscience should relate:

“The key point here is that by emphasizing a codetermination of both accounts one can explore the bridges, challenges, insights, and contradications between them. Both domains of phenomena have equal status in demanding full attention and respect for their specificity.”

We all know what pain is phenomenologically, what it feels like, but how to define it? The International Association for the Study of Pain offers this definition: “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” Of particular interest to neurophenomenology and embodied cognitive science is their claim that “activity induced in the nociceptors and nociceptive pathways by a noxious stimulus is not pain, which is always a psychological state.” Good that they do not try to reduce the experience of pain to the strictly physiological dimension, but I wonder how Merleau-Ponty, with his non-dualistic ontology of the flesh would have responded. Pain seems to transgress the border of mind and body categories, does it not? I am slowly biting off chucks of the work on pain at the Stanford Encyclopedia of Philosophy. Lots of provocative angles, including this one:

“there appear to be reasons both for thinking that pains (along with other similar bodily sensations) are physical objects or conditions that we perceive in body parts, and for thinking that they are not. This paradox is one of the main reasons why philosophers are especially interested in pain.”

Right now I am particularly interested in the spatial aspect of where pain seems to be, what I might label the spatial phenomenology of nociception. When I introspect on aching parts of my feet, it seems as if the pain occupies a volume of space. Using manual pressure I can find places on my feel that are not sore, right next to areas that are slightly sore, which are in turn near focal areas of highest pain. It seems as if the pain is locatable “down there” in my body, and yet what we know about the nociceptive neural networks suggests the phenomenology is produced by complex interactions between flesh, nearby peripheral nerves, the central nervous system, and neurodynamics in the latter especially. A way of probing this this would be to examine the idea that the pain experience is the experiential correlate of bodily harm, a sort of map relating sensations to a corresponding nerve activated by damage to tissue. So, is the place in my body where I feel pain just the same as where the damage or strain is? Or, Is pain caused by pain-receptive nerves registering what is happening around them, via hormonal and electrical signals? Or is pain actually the nerve itself being “trapped” or damaged, yet in a volume of undamaged tissue one can feel hurts? Could the seeming volume of experienced pain-space be a partial illusion, produced by cognizing the tissue damage as some place near or overlapping with yet not spatially identical to where the “actual” damage is, in other words a case of existential-physiological discrepancy? One scenario could be, roughly, that pain “is” or “is made of” nerves getting signals about damage to tissue; another would be that pain “is” the nerves themselves being damaged or sustaining stress or injury. Maybe pain involves both? Maybe some pain is one, or the other? In terms of remembering how my heel pain started, it’s not so easy, but I love to walk an hour or two a day, and have done so for many years. I recall more than ten years ago playing football in the park, wearing what must have been the wrong sort of shoes, and upon waking the next day, having pretty serious pain in my heel. Here are some graphics that, intuitively, seem to map on to the areas where I perceive the pain to be most focal:

from bestfootdoc.com

from setup.tristatehand.com

from plantar-fasciitis-elrofeet.com

If I palpate my heel, I become aware of a phenomenologically complex, rich blend of pleasure and pain. I crave the sensation of pressure there, but it can be an endurance test when it happens. Does the sensation of pressure that I want reflect some body knowledge, some intuitive sense of what intervention will help my body heal? How could this be verified or falsified? It is not easy to describe the raw qualia of pain, actually. I can describe it as achey and moderately distressing when I walk around, and sharp upon palpating. Direct and forceful pressure on the heel area will make me wince, catch my breath, want to gasp or make sounds of pain/pleasure, and in general puts me in a state of heightened activation. But I love it when I can get a therapist to squeeze on it, producing what I call “pain-pleasure”:

from indyheelpaincenter.com

This diagram below helps me map the sensations to the neuroanatomy. We need to do more of this sort of thing. This kind of representation seems to me a new area for clinical neurophenomenological research (indeed, clinical neurophenomenology in general needs much more work, searching for those terms just leads back to my site, but see the Case History section in Sean Gallagher’s How the Body Shapes the Mind).

from reconstructivefootcaredoc.com

What is producing the pain-qualia, the particular feeling? Without going too far into varying differential diagnosis, it is commonly attributed to plantar fasciitis.  There the pain would be due to nociceptive nerve fibers activated by damage to the tough, fibrous fascia that attach to the calcaneus (heel bone) being strained, or sustaining small ripped areas, and/or local nerves being compressed or trapped. A 2012 article in Lower Extremity Review states that “evidence suggests plantar fasciitis is a noninflammatory degenerative condition in the plantar fascia caused by repetitive microtears at the medial tubercle of the calcaneus.” There are quite a few opinions out there about the role of bony calcium buildups, strain from leg muscles, specific trapped nerves and so forth, and it would be interesting to find out how different aspects of reported pain qualia map on to these. Below you can see the sheetlike fascia fiber, the posterior tibial nerve, and it’s branches that enable local sensations:

from aafp.org

Next: fascia and the innervation of the heel, from below:

from mollyjudge.com

Another view of the heel and innervation:

from mollyjudge.com

Below is a representation of the fascia under the skin:

from drwolgin.com

There is a very graphic,under the skin, maybe not SFW surgeon’s-eye perspective on these structures available here. Heel pain turns out to be very common, and is evidently one of the most frequently reported medical issues. Searching online for heel pain mapping brings up a representation purportedly of 2666 patients describing where they feel heel pain: I can’t find where this comes from originally and can’t speak to the methodology, rigor, or quality of the study, but the supposed data are interesting, as is the implicit idea of spatial qualia mapping:  the correspondence of experienced pain to a volume of space in the body. It also quite well represents where the pain is that I feel. The focal area seems to be where the fascia fibers attach to the calcaneus, an area that bears alot of weight, does alot of work, and is prone to overuse. So, where is the pain? Is it in the heel or the brain? Is it in the tissue, the nerve, or both? Is there a volume of flesh that contains the pain? I am going to have to think about these more, and welcome your input. What about the central nervous system that processes nociceptive afferents coming from the body? A good model of pain neurophenomenology should involve a number of cortical and subcortical areas that comprise the nociceptive neural network: -primary somatosensory cortex (S1) and secondary somatosensory cortex (S2): -insula -anterior cingulate cortex (ACC) -prefrontal cortex (PFC) -thalamus Here are some representations of the pain pathways, or the nociceptive neural network:

from Moisset and Bouhassira (2007)

Moisett el (2009)

 

from Tracey and Mantyh (2012)

Broadly speaking, pain seems to be generated by tissue damage, inflammation, compromising the integrity of tissue, stress on localized regions, and so forth being processed by peripheral afferent pain pathways in the body, then phylogenetically ancient subcortical structures, and then the aforementioned cortical regions or nociceptive neural network.  As I have mentioned many times, making a robust account of how various regions of the brain communicate such that a person experiences qualia or sensory phenomenology will need to reference neurodynamics, which integrates ideas from the physics of self-organization, complexity, chaos and non-linear dynamics into biology.  It is gradually becoming apparent to many if not most workers in the cognitive neurosciences that there are a host of mechanisms regions of the brain use to send signals, and many of these are as time dependent as space dependent. Michael Cohen puts it thusly: “The way we as cognitive neuroscientists typically link dynamics of the brain to dynamics of behavior is by correlating increases or decreases of some measure of brain activity with the cognitive or emotional state we hope the subject is experiencing at the time. The primary dependent measure in the majority of these studies is whether the average amount of activity – measured through spiking, event-related-potential or -field component amplitude, blood flow response, light scatter, etc. – in a region of the brain goes up or down. In this approach, the aim is to reduce this complex and enigmatic neural information processing system to two dimensions: Space and activation (up/down). The implicit assumption is that cognitive processes can be localized to specific regions of the brain, can be measured by an increase in average activity levels, and in different experimental conditions, either operate or do not. It is naïve to think that these two dimensions are sufficient for characterizing neurocognitive function. The range and flexibility of cognitive, emotional, perceptual, and other mental processes is huge, and the scale of typical functional localization claims – on the order of several cubic centimeters – is large compared to the number of cells with unique physiological, neurochemical, morphological, and connectional properties contained in each MRI voxel. Further, there are no one-to-one mappings between cognitive processes and brain regions: Different cognitive processes can activate the same brain region, and activation of several brain regions can be associated with single cognitive processes. In the analogy of Plato’s cave, our current approach to understanding the biological foundations of cognition is like looking at shadows cast on a region of the wall of the cave without observing how they change dynamically over time.” But what of the original question? Is pain where you feel it in the body, or in the brain? It seems to me the answer must be both.  The experience of pain being localized there or a little on the left is a product of local tissue signals and receptor activation, which produces peripheral afferent nerve firing, which gets processed by spinal afferent neurodynamics, brainstem activation, thalamic gating, and then somatosensory, insular, anterior cingulated, and prefrontal cortical regions. Yet the real model of pain, one that invokes mechanisms and causes, remains elusive. And a good model of pain must account for the possibility of pain without suffering as well! For now, what I can offer are probes to get us speculating, thinking critically, and eventually building a clinical neurophenomenology of pain. If that interests you, by all means get involved.

A complex mapping of the interior sense: why Damasio’s theory of embodied cognition focuses on the brainstem and viscera

If, like me,  you are interested in the biological dimensions of cognition, consciousness, and phenomenology, you tend to study the cortex.  Attention, decision-making, having a sense of self, perception, visual awareness, and many other key higher mental processes are modeled with data from cortical measurements, and especially with recent neurodynamics and computational neuroscience, there are increasingly sophisticated theories about the underlying mechanisms. But the cortex possibly gets too much attention compared to the rest of the brain and body.  This is partially because it indeed makes us human, but also for practical reasons, much of what we know about the brain comes from EEG research that with people is usually limited to scalp-based cortical signal acquisition. Dig a little deeper, say, when learning about emotions, and the student or scholar gets at least cursory introduction into the sub-cortical, emotion-regulating structures of the limbic system such as the hippocampus, thalamus, and hypothalamus. Our sense of salience, that things matter, our bodily sensations, our emotions and drives are associated especially with these sub-cortical structures. The study of how the brain processes emotions and bodily sensations has pointed some psychologists, neuroscientists, physicians, and philosophers in recent decades towards the idea of the experienced, phenomenologically lived body as the basis of consciousness and the self (or “self”). The growing sense for some of us about the limitations of traditional computationalist/cognitive theories has led to to the idea that mind and brain must be understood as “enactive“: via  evolutionarily and environmentally situated, physiological, embodied processes that “bring forth an experienced world”. Whatever cognition is, more than a few of us cognitive scientists nowadays think of it as somehow based in temporally ongoing, fleshy, existentially meaningful conscious life, or phenomenology. The mechanics of embodied mind, and the embodied basis of phenomenology, are very poorly understood by cognitive neuroscience, psychology, and medicine. Only very recently has there been a revival of interest especially in how visceral body states get processed by the peripheral nervous system and subsequently transformed by the central nervous system. One could understand this as a subfield of neurophenomenology:  how the brain and body enable “the bodily feelings I have now”, the experiential phenomenology of the internal body (if you have poked around this site you may have seen my own 2011 dissertation work was on this very subject). The rise of interest in embodied cognition has been hugely advanced through the work of the neurologist Antonio Damasio. This pioneer of embodied cognitive neuroscience has been focusing the attention of the psychology and cognitive neuroscience communities on the brainstem as the basis of consciousness.  The brainstem is not the usual topic when scientists bravely try to model conscious aspects of cognition, and my sense is that in the public mind it tends to register mostly when someone famous has medical problems as a result of brainstem damage causing loss of core visceral regulatory processes, such as with the death of Michael Jackson. In Damasios’ account, it is not merely a bit player in the grand drama of how body produces consciousness, but plays a starring role. Damasio (2010) states in Self Comes to Mind:Constructing the Conscious Brain , “I believe that the mind is not made by the cerebral cortex alone. Its first manifestations arise in the brain stem . ” (p. 75).

Courtesy Wikimedia Commons

Above is the brainstem, in red.  It receives inputs from the spinal cord, called “afferents”, that deliver signals from sensory nerves distributed throughout the body. These sensory nerves are affected by the homeostatic and visceral states of organs, such as our heart beating, the fullness of our bladder, blood sugar levels, the gas exchange in our lungs, and so forth. How much of the time these nerve signals resulting from visceral processes enter into conscious is a murky business. Cognitive scientists and others researching consciousness have not particularly referenced interior body psychophysiology and internal body-sensation in most theories about consciousness, but the work of Damasio is changing that. In general, research on the perception of visceral states or “inner psychophysics” goes in and out of scientific fashion, according to Gyorgy Adam’s wonderful overview of many decades of research, Visceral Perception: Understanding Internal Cognition.

Courtesy Wikimedia Commons

Below is an MRI of a beating heart and other visceral organs, with the spine visible. Afferent nerves “encode” information (or “information”) about the homeostatic and other dynamics of these systems, and send signals to the spinal cord and brain.

Courtesy Wikimedia Commons

While the idea that the brainstem produces the first manifestations of consciousness may seem radical, Damasio cites experimental evidence that perception of visceral states is mediated by the brainstem’s nucleus of the solitary tract and the pons. This gives us a window into understanding interoception:  the awareness of our visceral organs and internal body (though I think interoception also refers to unconscious signals from bodily organs affecting the brain and possibly influencing unconscious cognition). Building on generations of basic research on the neurophysiology of visceral perception, Damasio (2010) defines interoception as a “complex mapping of the interior sense” (p. 97). He emphasizes this occurs through an interoceptive network involving significant processing by the brainstem, which, unlike a mere relay, receives, processes and integrates afferents from the state of the visceral organs, and in turn projects to the thalamus. Through the work of Damasio, Bud Craig and others, we can model cognition as based in a central nervous system which filters and transforms signals from the lifegiving organs of the body. Building on their contributions, here is how I understand the neurophenomenology of visceral perception to work: our body organs are responding to existential life needs, our brainstem gets signals from the body organs and actively filters and transforms the signals, and in turn projects to the thalamus. Thalamo-cortical fibers then make synapses with neurons in the insula, cingulum, and somatosensory and orbitofrontal cortices, regions implicated in interoceptive activity and cognitive processes handling internal body information.  These areas all contribute to both consciousness in the foundational sense Damasio is investigating, and also produces specific awareness of our emotions and of our interior bodily sensations, such as feeling hungry. What goes on at the final stage, when cortical regions take the transformed bodily signal from the brainstem and thalamo-cortical processing, and somehow produce changes in consciousness? That gets into very complicated territory, and nowadays some of our most progressive thinkers use ideas and mechanisms from physics, such as Walter Freeman’s work on cortical neurodynamics, or that of Varela and colleagues. As of 2013 the dynamical aspects of interoception do not seem to be on many people’s radar besides mine and maybe a few others. What does it all mean for theories about the mind? If we accept that thalamic relay nuclei, activated by processed bodily interoceptive inputs in the brainstem, engage in further processing, and subsequently synapse on to (probably) dynamically interactive interoceptive centers in the insula and orbitofrontal, sensory, and cingulated cortical regions, what do we then understand about consciousness and cognition? As far as I can tell, the heart of Damasio’s theory is that visceral and homeostatic body states are “mapped” on to the brain via the brainstem,  and this mapping is what consciousness and the sense of self is “made of”. As we are organisms needing to engage in the right sort of behavior to survive, we depend on our sensory and visceral organs functioning appropriately. Our minds are thus built out of an evolutionarily developed machinery of life preservation. Put another way: the interior chemical milieu in our viscera affects nerve signals into the brainstem, and brainstem-mediated afferent signals tell our brain and mind about the state of our organs by projecting to the “gateway of the cortex”: the thalamus. A series of cortical regions process the thalamus gated body-signals, some of which are  cognitively and phenomenologically processed by a person as more emotionally and behaviorally salient, such as signals associated with food and thirst, pain and sex, and fighting or fleeing. Damasio, never one to shy away from big ideas and bold claims, sums up the state of his thinking in a 2010 interview:

Feelings, especially the kind that I call primordial feelings, portray the state of the body in our own brain. They serve notice that there is life inside the organism and they inform the brain (and its mind, of course), of whether such life is in balance or not. That feeling is the foundation of the edifice we call conscious mind. When the machinery that builds that foundation is disrupted by disease, the whole edifice collapses. Imagine pulling out the ground floor of a high-rise building and you get the picture. That is, by the way, precisely what happens in certain cases of coma or vegetative state. Now, where in the brain is that “feel-making” machinery? It is located in the brain stem and it enjoys a privileged situation. It is part of the brain, of course, but it is so closely interconnected with the body that it is best seen as fused with the body. I suspect that one reason why our thoughts are felt comes from that obligatory fusion of body and brain at brain stem level.

Can we not agree, that this is a profound way of thinking about the human condition?   Buy me a beer!

Embodied cognition and overeating: a challenge for neurophenomenology and the public health system

Many people struggle with overeating. Body image issues influence people’s sense of worth and personal dignity. There is a great popular interest in understanding why it can be so difficult to get this aspect of our lives right. Scientists and doctors try to educate the public about the state of the current science, and about what is known. Modern scientific medicine has developed a way of thinking about disease and health that is holistic, inclusive, and integrative. There is a growing recognition that in the case of overeating, the list of causes are long, including attitudes about food coming from one’s childhood and upbringing, levels of energy expenditures, genes and hormones that regulate metabolism, neural networks in the brain activated when food is smelled, and so forth. Rather than emphasize any one cause, many scientists look at overeating in terms of a network of interacting systems affecting and affected by physiology, thinking, emotions, feelings, and behavior. This counters a historical tendency among hunger scientists to try to isolate a few particular hormones and signaling systems as the cause of overeating. This approach of reducing the complex to the simple has an amazing track record in the history of science, responsible for much of the modern world’s technical achievements. Scientific medicine attempts to understand illness and disease using this powerful “reductionistic” approach, which has produced countless innovations and therapies. Yet some systems in nature defy an overly mechanical understanding. The human body is not a car with faulty parts that can be identified as the cause of performance failures. Hunger can be understood as a bio-psycho-social product of body chemistry, psychological states and environmental context. Overeating involves a person’s experience of craving and not being sated as much as the physiological signaling of brain chemicals like dopamine or hormones such as ghrelin and leptin. Overeating is not just a system for science to investigate, it is a feeling involving thoughts and emotions and attitudes, as well as a behavior. Overeating involves disordered chemical signaling systems in the brain and body There does appear to be a fantastically intricate series of feedback loops and chemical signaling occurring when people get hungry and then eat but are not sated. Feeling “full” or satisfied is actually a complicated business where glucose (blood sugar) levels, brain chemicals such as dopamine, and a suite of hormones produce a network of changes that register in the mind as the feeling of wanting more food, or not. Blood glucose levels are regulated by insulin, but some people have a disorder in which the pancreas fails to produce sufficient insulin (Type 1 diabetes). Or, the cells may not take up the blood insulin correctly (Type 2 diabetes). Failure to metabolize blood sugar properly can influence the formation of adipose tissue (fat). The “metabolic syndrome” of disordered levels of blood sugar and hormones secreted by fat contribute to a person who has eaten plenty to still have cravings or not to feel satisfied. Fat cells secrete a protein known as leptin that acts as a signaling molecule. In healthy people, this hormone acts to inhibit appetite. One of the causes of obesity is from a failure to produce the right amounts of leptin, but sometimes the problem is more a failure to respond to proper leptin levels. In the healthy, leptin works in concert with another hormone named ghrelin, which is secreted as a person becomes hungry. After eating, ghrelin levels decline in a person with an appetite, metabolism, and levels of fat tissue that are regulated normally. Evidently it does not take much to knock these signaling systems out of balance. Obesity, diabetes and overeating disorders are at record levels. Stress, problems with work, romance and family life, the experience of loss and grieving, as well as aging change our metabolisms and leave us vulnerable to craving more than we need. Humans did not evolve in environments with triple bacon cheeseburgers and Super Big Gulps easily available, and the presence of such energy-intense, calorie-rich stimuli in our modern settings triggers our minds to crave what very few of us need. Treatments for overeating and binge-eating disorder Many people coping with eating disorders may alternate between periods of fad diets and binging, or intermittently exercising and then being sedentary. Over time, such sporadic efforts can easily lead to more weight gain. There are other options available, however. There is some evidence that the drug topiramate, also known for it’s anticonvulsant properties, can work as a treatment for overeating and binge-eating disorders. It’s mechanism of action is to dilate blood vessels and reduce activity levels of central nervous system nerve cells. Some people seem to be able to manage their unhealthy cravings for food better after this substance is administered. Denise Wilfley, PhD, is quoted in Psychiatry Online as reporting that “ample research has demonstrated that cognitive-behavioral therapy and interpersonal therapy can counter binge eating and lead to long-term weight loss”, though the benefits are modest. Empowered consumers and patients should not expect topiramate, a talk therapy, counseling or other potential remedies to be a “magic bullet” that cures the desire to binge eat. These therapies will typically deliver marginal improvements for most, though some may benefit more. A cost-benefit analysis is appropriate before trying any potential remedy. There is a complex relationship between the experience of hunger and it’s physiological basis. Science is still establishing some of the core principles that govern how genes, upbringing, diet, stress, attitudes, choices, brain hormones, blood sugar and environmental variables interact to affect the urge to keep eating. There are therapeutic options available for those who poorly manage the urge to overeat. Medication and/or talk-therapies may provide benefits, though individuals coping with the urge to binge eat should expect modest benefits in most cases. People managing this problem have considerably more resources than even ten years ago. While basic science moves forward slowly, there is ever more information available on how to recognize, understand and manage this problem than ever. The neuroscience of perceiving internal body states is proceeding incrementally. The genes that regulate metabolic chemical pathways and the networks of signaling molecules that activate and deactivate those genes are being discovered. Fat may be eventually understood as something like an organ that secretes molecules to regulate it’s own state. More here