Critical Neuroscience-Neurophenomenology in Psychiatry by Laurence Kirmayer, MD

clinical neurophenomenology, disease classification, history of neurophenomenology, medicine, psychiatry, psychology, symptom reports

Here is a thought provoking lecture on YouTube which investigates psychiatry’s problematic foundations, especially in terms of the influence of culture,  individual differences, and neurodiversity.

http://www.youtube.com/watch?v=PsubfDIKgUw Laurence Kirmayer is an MD at McGill University, and he has a lot to say about using clinical neurophenomenology to explore some very murky but important issues in psychiatry.  There really are problems that make psychiatry different from the rest of medicine, because however necessary the reductionistic-biological medical model nearly ubiquitous everywhere else may be, it is not sufficient. I’m very glad Kirmayer is bringing up Daniel Dennett and his work on heterophenomenological methods in the clinical context as well, not because it’s the end-all be-all, but because it orients what have historically been difficult and controversial debates  in an accessible, easy to read, reasonably pragmatic way. He is also doing good work in looking at how psychiatry gets it’s norms, methods, and foundational orientations, prompting him to call for phenomenological investigations in psychiatry. What a timely effort! I can’t help but feel the DSM-V was panned before it was published in 2013 (and not just by angry people with Asperger’s or Scientologists) because this phase of psychiatry may be running out of steam. The mapping between biological mechanisms to the myriad ways individual people in various cultures live out their emotional pain and existential struggles isn’t good enough.  The ontology or foundational ideas about a psychiatric patient must reference existential reality: the meaning of embodiment and how one’s experience brings forth a lived world, while the ontology of neuroscience is based on genes, proteins, signals, action potentials, circuits, modules, information-processing, and maybe even dynamical systems. Current psychiatry seems to me to be inadequately addressing the foundational problem of how to map these domains. All the genome-wide association studies, connectome diagrams, and brain imaging data in the world aren’t enough to create diagnostic categories that cluster the lived meaning, experiences and embodiment of similar bipolar or schizophrenic patients together, and that of dissimilar patients apart. There really is alot of applied work needing to be done on how to model the cognition of patients whose disorders manifest as disturbances of body cognition or existential crises (here’s my version, dealing with heartbeat perception). Moreover, foundational investigations into the ontology of psychiatry may very well provide a needed stimulus to get psychiatry out of it’s current funk betwixt and between medical humanism as a healing art, and bio-reductionistic techno-medicine. Overall I am convinced clinical neurophenomenology is a vital and largely new area, despite the pioneering efforts of the neuropsychiatrist Erwin Straus and the more recent work of neurologists such as  Oliver Sacks and Antonio Damasio. The lodestar of clinical neurophenomenology seems to me to be Varela’s idea of a mutual constraining and mapping between data from lived, embodied phenomenology and theories based on cognition and neuroscience. There is a more about Kirmayer at http://www.mcgill.ca/trauma-globalhealth/people/canada/kirmayer/

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

body knowledge, clinical neurophenomenology, embodiment, interoception, introspection, introspective accuracy, medicine, pain, physiology, symptom report accuracy, symptom reports, visceral perception

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 bestfootdoc.com

from setup.tristatehand.com

from setup.tristatehand.com

from plantar-fasciitis-elrofeet.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

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

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

from aafp.org

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

from mollyjudge.com

from mollyjudge.com

Another view of the heel and innervation:

from mollyjudge.com

from mollyjudge.com

Below is a representation of the fascia under the skin:

from drwolgin.com

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: heel pain mapping 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) "Brain imaging of neuropathic pain"

from Moisset and Bouhassira (2007)

Moisett el (2009)

Moisett el (2009)

 

from Tracey and Mantyh (2012)

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

body knowledge, clinical neurophenomenology, consciousness, embodiment, interoception, physiology, visceral perception

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

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 of Wikimedia Commons

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

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! Donate Button

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

clinical neurophenomenology, medicine, physiology, psychiatry, psychology, visceral perception

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

Verbal report data: psychologists may be skeptical, but clinicians are more practical

clinical neurophenomenology, cognitive science, introspection, medicine, symptom reports

Cognitive neuroscience and psychology needs to account for  verbal report data from people about their body states. In perceptual psychology and psychophysics experiments, in cognitive studies of human problem-solving, in clinical trials of drug efficacy and safety, in phenomenological-psychological investigations into the thematics of body experience, researchers routinely ask subjects or patients to answer questions. This is so common that its significance is perhaps under-appreciated. Science, at least in a narrow sense,  is conventionally understood to be based on objectively observable facts, not subjective opinions. But certain phenomena can not only be observed from the outside, as part of a system, but can also be reported on by people from the inside, as perceived or experiential events.

This regular use of the human self-reporting capacity is more remarkable in the light of intellectual history.  “Orthodox” cognitive science developed in the era of behaviorist dominance, and inherited certain skepticism about the trustworthiness of verbal reports, which are viewed as being sources of data, but not “privileged.” This stance indicates a rejection of older philosophical and psychological traditions that emphasized the use of introspection. Nonetheless, even in the time of behaviorist hegemony, psychologists still asked subjects questions in perception experiments, and clinicians have always used patient assessments to gain insight (Nahmias, 2002). While certain path-breaking cognitive scientists and psychologists explored the nature of introspection, and worked out the circumstances in which verbal reports could be authoritative and true accounts of aspects of cognitive processes (Erickson and Simon, 1991), (Ericsson, Chase, and Simon, 1979), the results of other widely cited experiments have been interpreted to denigrate introspective data, especially that of Nisbett and Wilson’s (1977) “Telling More than we can know” paper. Their research has been interpreted to indicate, for instance, that subjects made demonstrably inaccurate judgments about their underlying mental states because human beings apparently have little or no direct introspective access to the underlying cognitive processes of the mind (pg. 233):

The accuracy of subjective reports is so poor as to suggest that any introspective access that may exist is not sufficient to produce generally correct or reliable reports.”

The interpretation of their data featured assertions that are now influential:  subjects lack  introspective access to the causal relationship between stimuli controlled by the experimenter and the verbal reports they produce. They are unable to accurately report which stimuli affected their responses. Rather, these verbal reports of effects of stimuli are based on unvalidated belief (such as naïve “folk psychological” theories about the causal connections between the stimuli and their response). Furthermore, if the reports on stimulus-response relationships are correct, it is because their naïve theories happen to be correct, and not because introspection gave them any privileged access to information. The upshot can be summarized as: subjects in situations with variables controlled by scientists make introspective judgments about why they behave in a particular manner or think a certain way, they state this explanation verbally to an experimenter, who can show the explanation to be false: (pg. 243)

“In order to test subject ability to report influences on their associative behavior, we had 81 male introductory psychology students memorize a list of word pairs. Some of these word pairs were intended to generate associative processes that would elicit certain target words in a word association task to be performed at a later point in the experiment. For example, subjects memorized the word pair “ocean-moon” with the expectation that when they were later asked to name a detergent, they would be more likely to give the target “Tide” than would subjects who had not previously been exposed to the word pairs….Immediately following the word association task, subjects were asked in open-ended form why they thought they had given each of their responses in the word association task. Despite the fact that nearly all subjects could recall nearly all of the words pairs, subjects almost never mentioned a word pair cue as a reason for giving a particular target response. Instead subjects focused on some distinctive feature of the target (“Tide is the best-known detergent”), some personal meaning of it (“My mother uses tide”), or an affective reaction to it (“I like the Tide box”).

The influence of this research has had the practical effect of renewing suspicions among psychologists and other researchers about introspective data, even if such methods continue to be used (Jack and Roepstorff, 2003) and despite the balanced view of Nisbett and Wilson where introspection has some utility regarding “sensations and/or private facts”, which takes into consideration the longtime use of introspective data as a method in psychology. Cognitive scientists, psychologists, physicians, and others can adopt their pragmatic distinction between the contents of cognition, such as sensations and emotions which can indeed be known and verbally reported, and the underlying causes, the information-processing or cognitive processes, which remain epistemologically inscrutable to introspection.

Yet while clinical medicine often regards introspective data with caution, it nonetheless uses it pragmatically. For instance, the standard neuropsychology text Clinical Neuropsychology (Heilman and Valenstein, 2003) states (pg.5)

at times, patients’ observations of their own mental state may not only be helpful but necessary.”

This implies that it is a standard clinical methodology to use introspective data, and that patients have some useful access to their own minds.

This data-collection method of asking subjects and patients for self-reports is routinely used, according to psychologist Arthur Stone (Stone, 2000) (pg. 297):

“In both clinical practice and in research, the primary method of obtaining information about physical symptomology is through self-reports. Every day, thousands upon thousands of health care providers ask their patients to describe how they are generally feeling and too discuss specific symptoms. Patients present their doctors with panoply of global states (“I feel lousy,” “I am fatigued,” “I don’t feel right”) to very concrete descriptions (“I have a sharp pain in my right knee that is worse on awakening”). Information from these interviews, along with various medical tests, provides the basis for treatment and for the evaluation of its efficacy. In medical research, information of the same sort is obtained with questionnaires and structured interviews. These data-collection methods may provide a more systematic way of gathering physical symptom information, but regardless of the mode of data collection, the information is self-reported. Thus, reports of physical symptoms may be considered the mainstay of medical practice and research”

the legacy of Cartesian “objectivity” makes it hard to understand patient verbal reports

clinical neurophenomenology, embodiment, introspection, medicine, symptom reports

Psychiatrist Allan Beveridge (2002) hones in on a facet of the patient-physician relationship relevant to neurophenomenology: the over-adoption in medicine of the scientific attitude of objectivity towards phenomena. While entirely appropriate in the many research contexts, this may make understanding the personal body-knowledge of the patient more difficult (pg. 101):

In the mental state examination, a standard method of describing the clinical encounter is to contrast the patient’s supposedly ‘subjective’ account with the doctor’s ‘objective’ description. In this model, the doctor is granted a privileged position: the clinician’s perspective is taken to be superior to that of the patient. The doctor’s objective approach is considered neutral, scientific and representing the truth of the matter. In contrast, the patient’s subjective report is regarded as unreliable, distorted and potentially false. The lowly status of the subjective perspective is further emphasized by the frequent use of the accompanying prefix, merely. On reflection, this dichotomy is an extraordinary one. It is held that the doctor is an authority on the patient’s inner experiences. The doctor knows more about how the patient is thinking and feeling than the patient him-/herself

This “scientific” medical stance towards patient subjective reporting is consistent with the Cartesian heritage of the sciences of the mind. The implications, hidden or unexamined commitments should be critically examined if the verbal reports about patient body-states are to be better grasped by science and medicine. To the extent cognitive science, psychology, neuroscience, and medical fields uncritically base their methodologies on unexamined premises, certain problems may appear just due to the very choices of what is considered “data”. The relegation of patient verbal reports to the category of “merely subjective” allows for Cartesian assumptions about cognition to create difficulties at the outset of any research project attempting to model personal knowledge of the body. It may be that the very categories of subject and object, or scientific knowledge vs. subjective or “folk psychological” naïve theories of the body, present foundational problems for understanding how neurophysiological processes relate to verbally reportable knowledge of the body. But as a practical matter, health care professionals must simply cope with patient statements as one more data source (Ersser and Atkins, 2000, pg. 68):

Clinical decisions involve information of a necessary type and quality. Professionals take account of both objective and subjective data during the clinical assessment process to decide on a patient’s health care need and care plan. The difficulty lies in professionals understanding how best to reconcile their objective perspective with that of the patient, when formulating clinical judgments

Before a doctor revives technical training, he or she is a person with experiences of health and sickness. The verbal reports of patients are interpreted by professionals with their own history of embodiment. To what extent does their personal body knowledge consciously or unconsciously affect their clinical intuition about the accuracy of patient verbal reports? Does expert knowledge of the body gained from studying anatomy and physiology allow for better knowledge of one’s own body? Such questions point to our current rather murky understanding of embodied cognition, underscoring the need for models capturing richer, more subtle aspects of experience, cognition, and brain.

Gallagher and Coles on body schema vs. body image and the body percept

clinical neurophenomenology, embodiment, medicine

The philosopher Shaun Gallagher has collaborated with neurologist Jonathan Coles on the significance of patients with enigmatic body-knowledge problems (Gallagher and Coles, 1998).  Gallagher has analyzed this clinical data in the light of phenomenology and neuroscience, and has  an essential book  for anyone interested in neurophenomenology: How the Body Shapes the Mind

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Gallagher is formulating a sophisticated take on embodied cognition that redresses the relative lack of attention by Varela and others to clinical studies of body knowledge disorders .  I have believed for some years that the wealth of neurological case studies  presenting puzzling data needs more focus in neurophenomenology. Since the early 20th century, numerous patients with body knowledge based disorders and pathologies have come to light, leading to the notion of a body schema (Head and Holmes, 1911), which Gallagher and Coles (p.372) say involves:

“…a system of motor capacities, abilities, and habits that enable movement and the maintenance of posture. The body schema is not a perception, a belief, or an attitude. Rather, it is a system of motor and postural functions that operate below the level of self-referential intentionality, although such functions can enter into and support intentional activity. The preconscious, subpersonal processes carried out by the body- schema system are tacitly keyed into the environment and play a dynamic role in governing posture and movement. Although the body-schema system can have specific effects on cognitive experience…it does not have the status of a conscious representation or belief”

Gallagher and Coles maintain that progress in understanding embodied cognition requires a distinction between this body schema and the notion of the body image (p.371):

“The body image consists of a complex set of intentional states-perceptions, mental representations, beliefs, and attitudes–in which the intentional object of such states is one’s own body. Thus the body image involves a reflective intentionality. Three modalities of this reflective intentionality are often distinguished in studies involving body image:

(a) the subject’s perceptual experience of his/her own body;

(b) the subject’s conceptual understanding (including mythical, cultural, and/or scientific knowledge) of the body in general; and

(c) the subject’s emotional attitude toward his/her own body”

Gallagher emphasizes the wide variety of ambiguous and contradictory ways these terms have been used, and while noting some critics have proposed that deploying new terms could eliminate such confusion, he labors to develop a dependable, standard use of the technical terminology that can serve to make sense of clinical neurophenomenology such as that of the patient I.W, who suffered damage to nerves below the neck. This man now has to consciously will in order to perform actions people normally take for granted (p. 374):

“Maintaining posture is, for him, an activity rather than an automatic process. His movement requires constant visual and mental concentration. In darkness he is unable to control movement; when he walks he cannot daydream, but must concentrate constantly on his movement. When he writes he has to concentrate on holding the pen and on his body posture. IW learned through trial and error the amount of force needed to pick up and hold an egg without breaking it. If his attention is directed toward a different task while holding an egg, his hand crushes the egg”

The usefulness of the crisp distinction between body schema and body image becomes apparent when trying to explain the patient’s body experience and body knowledge (though Gallagher states that there is not in fact such a simple distinction possible in many cases). Normal people can perform such acts without much explicit attention, which is to say such common actions are enabled by the subconscious processes characterizing the body schema. I.W, on the other hand, must carefully and consciously go through the necessary steps to perform everyday acts. Adopting Gallagher’s distinction, we could say in the absence of the unconscious body schema, the patient must now depend on his conscious body image. To the extent this distinction is true; it should help a great deal in unpacking the various meanings of body-knowledge.

symptom verbal reports and existential-physiological discrepancy

clinical neurophenomenology, interoception, introspection, medicine, symptom reports, visceral perception

While the anatomical basis of how nerve projections enable perception of the body is rather well known, physicians confront situations where patient verbal reporting about symptoms does not match models based on neurophysiological mechanisms. For instance, the Merck Manual Medical Library (2009) states:

“Painful stimuli from thoracic organs can produce discomfort      described as pressure, gas, burning, aching, and sometimes sharp pain. Because the sensation is visceral in origin, many patients deny they are having pain and insist it is merely discomfort”

The Mayo Clinic Heart Book (Gersh, 2000) describes the concept of uncomfortable feeling of thumping inside the chest known as palpitations, but does so from the point of view of patients (pg. 38):

“Although the apparent cause of the thumping in the chest would seem to be the heartbeat, this is not always the case. Some people have a normal heart rate during their palpitations. Presumably, they are either anxious or experiencing chest wall twitching that is mistaken for heartbeats”

Situations where the “folk physiological” (see Churchland, 1989, for a description of expert knowledge vs. folk beliefs) understanding of the body is apparently falsified by science can be labeled examples of existential-physiological discrepancy (Laughlin, McManus, D’Aquili, 1990). Mismatches between body-as-experienced compared to the “objective body” of scientific medicine and physiology (including the feeling of “phantom limbs” by amputees) are based on the idea that people may often have very limited “true” access to physiological processes. A more commonly presented variant or subset of this principle is the idea of “referred pain”, where the region causing understood to be causing the pain is spatially removed from the area where the patient senses it.

The Merck Manual (2009) gives an example: sometimes pain felt in one area of the body does not accurately represent where the problem is, because the pain is referred there from another area. Pain can be referred because signals from several areas of the body often travel through the same nerve pathways in the spinal cord and brain. For example, pain from a heart attack may be felt in the neck, jaws, arms, or abdomen. Pain from a gallbladder attack may be felt in the back of the shoulder.