Reset your brain and body for a pain-free life.

Joe Tatta, PT, DPT


Pain and the Neuroscience of Nociception with Dr. Tor Wager, PhD

Welcome back to the Healing Pain Podcast with Dr. Tor Wager, PhD

Pain goes beyond what we physically feel in our bodies. It reaches back into other aspects—from the mental to emotional. Take a deeper dive and explore the neuroscience of nociception and the perception of a painful stimulus with Dr. Tor Wager, director of the Cognitive and Affective Control Laboratory and Professor of Psychology and Neuroscience at the University of Colorado, Boulder. He talks about the factors that influence pain as well as the facts or myths about pain as a learned experience. Also, learn where the experience of pain comes from and the functions it serves while tracing the relationship between emotion and pain. Find out why exposure to pain may be the fastest way to overcome and alleviate it.

I’m excited to share this great information about integrated pain care and pain science. I’ve received a lot of emails wanting to know more about the neuroscience of pain or simply what is known as pain science. What’s interesting about this request is that both practitioners and those with pain are hungry to learn more. I started to discuss this topic on episode 97 when I spoke with a physiotherapist, Dr. David Butler, about the biopsychosocial model of pain. In episode 92, we explored the Neuromatrix Theory of Pain with Dr. Timothy Salomons. In this episode, we’re going to take a deeper dive and explore pain and the neuroscience of nociception or what is known as the perception of a painful stimulus.

Joining us to discuss the neuroscience of pain is Dr. Tor Wager. Tor is the Director of the Cognitive and Effective Control Laboratory and Professor of Psychology and Neuroscience at the University of Colorado. His research focuses on the brain mechanisms, underlying expectations, and placebo effects and their influences on brain systems involved in pain, emotion, and motivation. He is also actively involved in the study and research of the emerging field of brain-body medicine. On this episode, you will learn where the experience of pain comes from and what functions it serves, more about the pain neuromatrix as well as brain circuits that generate pain. What the relationships between emotions and pain are, why pain is a learned experience and the steps you can take to unlearn your pain. Finally, how exposure to pain or exposure therapy may actually be the fastest way to alleviate pain.

In this show, we can often get a little technical regarding pain science. I’m always interested in taking complex theories and turning them into simple and actionable lessons you can use in real life. With that intention, I’ve created a great freebie that you can download and complete on your own and help alleviate your pain. This is a brief exercise based on mindfulness, acceptance and commitment therapy, and it’s simply called, Notice What You’re Thinking About Your Pain and Anchor In. This exercise is so simple that each time I give this to one of my patients to help them with unpleasant thoughts or feelings or emotions about pain, they love it. They can’t believe how easy it can be to create some space from these unpleasant sensations. To download this Freebie, text the word 102DOWNLOAD to the number 44222 or you can open up a browser on your computer and type in the URL

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Pain and the Neuroscience of Nociception with Dr. Tor Wager, PhD

Tor, welcome to the show. It’s great to have you here.

It’s nice to be here.

In our previous episode, I had Dr. Tim Salomons who, like yourself, is a neuroscientist and psychology researcher. He talked a lot about the pain neuromatrix and things we’re learning from the research that everyone’s doing on the neuromatrix. Can you share some of the latest updates from your lab about what we’re learning as far as looking into the brain and pain neuromatrix? What are some of the latest findings?

We’re learning a lot about the pathways that generate pain and help to shape and regulate pain under different circumstances. One of the things we’ve been focusing on a lot is developing models of pain in the brain that can track and predict what somebody is going to experience. The magnitude of their pain experience and are they experiencing pain or not at a given time. Our goal is to understand how the brain generates pain, what are the factors that contribute and how can different kinds of interventions help, whether there are drug interventions or psychological interventions or behaviors like exercise. We want to develop models that can track pain quantitatively because that can give us an idea about the systems involved. It’s all about decomposing those systems.

What we’re learning is that there are multiple pathways in the brain that contribute to pain experience under different circumstances. There isn’t one thing that is pain under all circumstances for all people. There are multiple systems that contribute to the brain. That gives us ideas that for different people, pain might be coming from different sources in the brain. You might have sensitization in neural pathways in different systems of the brain which have different implications for treatment and for what’s wrong with a given individual person. That can help us understand how to help.

We’re getting a better handle on the systems that track, capture and evoke pain for a given person. By evoke pain, I mean if you have a stimulus, it could be something that’s painful like holding a hot cup of coffee. It’s painful but tolerable or getting pressure maybe on your thumb or another part of your body. We’ve been testing other kinds of data sets too. It could be electrical, a painful but safe shock. There are other models of visceral pain, it could be like models of intestinal pain in the stomach or the GI tract or the esophagus. With our collaborators, we’ve tested all of these kinds of evoked pain. This is a feature of chronic pain because many people with various chronic pain conditions have hypersensitivity to some subset of those stimuli. They might also have what’s called allodynia where something that’s normally nonpainful like light touch becomes painful.

We’re developing models for both pain and there is a canonical system in the brain that responds in a very consistent way across individuals. It tracks the level of pain people experience when they get those kinds of stimuli. That’s consistent. Some of the regions that are involved are things that we would expect from other animal and human work, like the spinothalamic tract. Parts of the ventrolateral thalamus and the posterior insula and somatosensory cortex. There are so-called Medial Pain System, so medial thalamus in the anterior cingulate cortex as well as the mid and anterior insula and other parts of the brain to respond and help track pain.

HPP 102 | Neuroscience Of Nociception

There are multiple pathways in the brain that contribute to pain experience under different circumstances.


We’ve been publishing studies that develop such models on a subset of individuals, mostly healthy individuals, and then test them on different individuals. We had one particular pattern that we call the Neurologic Pain Signature. The journal editors asked us to call it that and we discussed the name but it stuck. It’s important because you want to have a thing that you can test across individuals. We’ve tested that on many samples to see whether it responds to painful events of all types I just described. Does it track pain intensity? Does it correlate with pain in individuals? It does in about 90% to 95% of the individuals. We can get up a positive hit for, “Yes, this thing tracks your pain,” to some degree.

We had a paper come out on neurology and that’s a test of that pain signature on 600 people from twenty different studies around the world. About 95% of people have this pattern response to painful events. We’ve also been very interested in placebo effects and other things that might shape pain like people’s expectations, beliefs, as well as drug treatments. All of these twenty studies were studies of placebo effects. They all got a condition where people got a fake analgesic cream that they were told was a real analgesic essentially. People believed it and they report lower pain. There’s a control condition that’s comparable to compare that placebo cream too. Virtually, in all of those studies, there is a significant reduction in pain when people got the placebo treatment, but there was a very little reduction in the pain signature.

That helped tell us both that this particular brain pattern is responsive to pain across a variety of different groups around the world and different types of pain. It’s very hard to move up and down by manipulating expectations and beliefs. There are a whole series of other publications that were smaller and not 600 people that show and in different ways that it’s not very sensitive to changes, whether you reappraise pain, imagine it’s terrible or imagine it’s better. It’s tracking one ingredient of pain. It’s tracking the nociceptive pain that’s induced by the stimulus.

We’ve done studies and other people had to that look at top-down influences. If people get a placebo treatment and they expect less pain, they will very reliably report less pain. We have other paradigms where we’ve given people information that, “This is what other people thought this pain felt like. Other people thought this was bad. Other people thought this wasn’t so bad.” That produces very reliable influences on what people feel. It also produces reliable influences on their autonomic nervous system. Your skin sweats more and your heart beats faster if you believe something is going to be more painful, but we don’t see changes in this particular brain system that are very large and in these cases either.

This gives us a measure of nociceptive influences on pain that is very reliable across people. It doesn’t mean everybody’s exactly the same, but it means it’s a consistent core system. It doesn’t track a number of things. It does track drugs. Opioid drugs were tested and they do influence this system. Other kinds of reevaluation and placebo effects don’t have big influences. There are other systems that also contribute to pain that are important.

It’s a great introduction to what we’re going to talk about, but to rewind and go over one or two points, in this study of 600 people, these are people without chronic pain. Is that correct?

Yes. They’re all called neurotypical. They were community samples and some of them are student samples or college students.

When you elicit a response, for instance, get them a little pinprick, you see the same pattern fire or the same “signature” happening in their brain. Do we have any information or any research on signatures at a specific a diagnosis?

That’s a direction that we’re heading and that’s the direction that other people are heading too. Our idea about this is that we’re targeting this experience and that’s part of a diagnosis, but it’s not the same as a diagnosis of chronic pain. We also have a whole series of studies testing the specificity of this particular pain signature. It doesn’t respond to other kinds of emotional events, observing other people in pain, looking at pictures that are aversive or even hearing aversive sounds. We’re testing that. It doesn’t track the intensity of the aversive sounds or their tastes. We’re testing other things.

The profile is very specific. If you think about that relationship between those evoked experiences in chronic pain, chronic pain is much more complicated because it’s also about the whole person. You get a diagnosis of chronic pain by experiencing persistent pain. They can come and go, but it’s ongoing for more than three months or some reasonable cutoff. That’s about the person and not about the experience at any given time. When you try to track that in the scanner, is there something that sensitive and specific to a diagnosis of chronic pain? That’s where we don’t have any validated measures that I know of.

Just because you’re seeing the pathways light up and fire, it doesn’t necessarily mean that pain is being elicited?

Yes, that’s right, although it tracks the immediate experience of pain. Our pain patterns are tracking it well. There’s another system that seems to track the influences on pain that are related to your beliefs and your assessment of the significance of the pain. Even if that tracks experience well, it’s not clear that that tracks people’s ongoing clinical pain when they say, “It just hurts all the time.” It’s not clear yet how similar that evoked pain pattern is to what’s driving people’s ongoing experience. That might be an even more complicated mix of things. The literature so far shows that there is a relationship. When people have this hypersensitivity or allodynia, there are very similar areas to those we’ve been studying and finding that respond.

When you say, “That hurts a lot more because you touched my affected limb and it’s terrible.” It doesn’t seem in some other studies, to track ongoing chronic back pain very well and maybe some other forms of ongoing spontaneous pain or clinical pain that fluctuates up and down. That might be driven by different systems and that also might be more variable across different people. There’s a relationship with the systems we’re studying, but I don’t think it’s the whole story in terms of explaining people’s ongoing chronic pain and discomfort.

One example is a study that we published about fibromyalgia. What we found, in brief, is that people with fibromyalgia were hypersensitive to pressure pain. That makes sense. That’s a feature of fibromyalgia, but it’s not the whole story. We found that their brains, in particular, this pattern that we’ve been studying and characterizing across samples, is also hypersensitive. We see an increase in sensitivity in the brain to pressure but not for everybody. It wasn’t like all the patients are way above all the controls. There is some effect. That was part of the whole thing. We also tested different brain responses to a different stimulus, which is a multisensory stimulus. It’s flashing checkerboards, lights and tones, things that the fibromyalgia patients found aversive, but controls don’t find to be aversive.

There we found brain differences as well that were quite large effects. When we put those things together, we could tell who had fibromyalgia in the sample and who was in control with a little above 90% accuracy. That’s a case-control demonstration. That, “Yes, there’s something really different in the brain that tracks it.” One of the next frontiers is specificity. Do we know that only fibromyalgia patients have this particular feature in the brain? I doubt it. It’s probably a feature of multiple different disorders. These brain changes probably cut across our current diagnostic categories because our current diagnostic categories are not very good at determining what kinds of treatments people should get. They’re probably not biologically real categories in the first place in some sense.

I know a lot of your work centers around learning and the idea of unlearning pain. Can you talk a little bit about the fact or myth around that pain is a learned experience? How does that mean to someone who hears that? It’s like, “I didn’t study to be in pain, and somehow this happened to me.” What’s the stimulus?

We’re using the word learning in a different way than you think of. It’s not like going to school and learning something or you studied for it. It’s grounded in this idea that your brain is constantly learning from every experience that you have. Imagine that you go to a new place and you see a beautiful fountain in the city, in Oslo or something. You’ll remember that for years. Your brain has laid down a memory. There are different kinds of memories that get laid down in different systems in the brain. As far as I know, every neuron in your brain and in your spinal cord learns from experience.

It changes its firing as a function of what experiences it’s had in the past. Your brains are constantly learning. One of my favorite examples is from a colleague James Grau in Texas. He’s been studying the spinal cord for fifteen years or more in rats and how the isolated spinal cord can learn to walk over or step over an obstacle and that’s even without the brain. The spinal cord is this incredibly complex set of neural circuitry. We don’t think about it as a learning system, but it absolutely is. Your brain is always learning. Some of the things that we know is that giving people experiences like where you have one set of cues or context, where you’re in one place and you experienced something that’s very painful and in another place, you experienced things that are not that painful. Your brain encodes that context or those cues and then it will create a lot of fear if you’re in a setting with a lot of pain. That’s a learned response as well.

HPP 102 | Neuroscience Of Nociception

There are different kinds of memories that get laid down in different systems in the brain. Every neuron in your brain and in your spinal cord learns from experience.


Secondly, that context will enhance the pain. If pain is predicted, in our human studies, people experience more pain. In contexts that are safer, they experience less pain. We’ve done a number of laboratory studies where we can show that. When we give people the right kinds of experiences, just those cues alone can amplify or diminish pain. They can also amplify or diminish the autonomic responses very reliably. These include heart rate and skin sweating. Essentially, that’s a learning effect. Learning, in this case, subsumes a very broad class of different kinds of changes in the brain that are largely mediated by neuroplasticity.

After an injury, a person who develops chronic pain may have sensitization or learned amplification of activity in systems that carry pain-related information to the brain and in other systems in the brain itself. All of those are learned but not consciously by the person, they’re adaptive changes in the brain to that experience. There was a powerful and thought-provoking set of animal studies that have been done by a number of groups over the past years, including people like Jing Wang, Marco Martina, Vania Apkarian, Jim Surmeier, Rohini Kuner and Stephen Waxman. What this literature shows is that depending on the type of pain challenge or model, if you have a partial nerve injury that creates chronic pain behavior in virtually all rats, there are some very reliable increases in neuropathic pain. There are changes in the brain in a number of circuits, so the spinal cord can sensitize.

Even if the peripheral injury has healed and is no longer a problem, the spinal cord is still signaling amplified pain. What might even be normal touch-related signals might trigger that amplified pain. It doesn’t end in the spinal cord, some other studies have shown amplified activity in the amygdala, which seems to be necessary and sufficient for maintaining the chronic pain in some cases. You can get amplification and the amygdala and that work was done by, for example, Yarimar Carrasquillo, Robert W Gereau, Volker Neugebauer, a group of scientists and others. You can even get sensitization of the amygdala, which might be related to fear. It might cause fear or amplification of pain behavior that’s not about the primary nociception, but it’s about it’s about the aversiveness of pain.

There are changes in another brain area sometimes called the reward center called the nucleus accumbens, which is important for determining what an animal or a person will approach or avoid. It’s a motivational center. There are changes in that center which seem to mediate a withdrawal, a depression-like behavior within animals. There are withdrawal kinds of behaviors and in some cases, increases in pain behaviors or pain sensitivity as well. There are changes in the thalamus and there are changes in a bunch of other brain regions too.

You can get these learned adaptive responses after an injury that can maintain pain in animals in a number of different ways. When we think about learned pain and about what’s happening, if you have pain in your knee or your back, is it just in your back? Probably not. There’s probably some contribution of sensitization in the nervous system above and beyond what’s happening in the back. Even if the back has healed or you did the perfect surgical intervention or whatever, there’s nothing you can do to the back that’s going to help with that central sensitization potentially for some people.

It makes me think of a little bit about some of the research around anxiety and on the factors about learning and unlearning. I guess working toward extinction, do we have some data yet that we can help people unlearn and make this experience in their brain extinct, which would, in essence, flip the switch and turn pain off?

There are practices that can be very effective for a lot of people to help extinguish or reverse some of that central sensitization. Sometimes these things have many flavors. There are probably 300 different named treatments for chronic pain and also for mood disorders. There are 300 flavors, but there are some common principles that cut across all of these treatments. Some of these things are built as amazing new treatments that nobody’s ever done before. Some of them are standard practice, but these principles are operative across a lot of them. One of the important principles is exposure to something that’s potentially painful. One of the things that seem to happen when pain chronifies is people think the pain is a sign of damage or danger. “If I do anything painful that’s going to be bad for me and I’m going to injure myself more, I’m going to avoid doing that.”

That has multiple negative impacts and we’re still understanding what those are. There are systems in the brain that seem to be important for chronic pain, not immediate pain experience right now or evoked pain, but the chronic pain seemed to be systems that are involved in avoidance learning. Maybe your back is actually sending normal signals now, but what’s happening is that your brain is saying, “I better pay attention to that signal. I better pay attention to that sensation. I better be afraid of that. I better not do things that are associated with that.” That, in a sense, maybe a big part of what maintains pain for some people.

Sometimes moving or doing something that’s painful could reinjury you. That’s a judgment call that you have to make with a pain specialist, hopefully. For a lot of people, that’s a mistaken belief and they don’t need to avoid anything that hurts. One of the things that pain specialists from multiple disciplines do is they start to do exposure. They say, “You can do that. It hurts? That’s okay, you can do that. It will hurt to some degree, that’s okay and that’s normal.” They can give people the confidence that that’s true. When you switch from avoiding anything that might be painful to engaging and even experiencing pain as a normal part of the recovery process, the learning and plasticity in those systems that say, “Alarm bad, terrible, terrible,” that starts to go away because you’re teaching your brain, “That’s not something terrible. That’s normal and expected. I can do that thing.”

What might be happening is we’re reversing some of the maladaptive plasticity in those circuits involving the nucleus accumbens and other areas of the brain. In some places, exposure to pain as a first line treatment. A lot of people who work in physical therapy and physiatry, that’s also some of the things you’re going to focus on. Expert guidance into what’s safe and let people know what’s safe and that they can engage in that. It also might be important to have normal sensory experiences. Our brain’s constantly adapting to the level of sensation that we feel. Doing activities that give you sensory stimulation or motor simulation, even if it’s painful, can help to normalize those sensations. That’s an ongoing area where we’re learning more scientifically.

Just a quick analogy, all of our sensory systems adapt to the level of input. If you’re in a noisy environment and there is a lot of noise around you, even in your ears, the cells in your cochlea adapt and they become less and less sensitive to loud noises. All of our senses are tuned to that dynamic range. Pain probably works the same way. If you were in a terribly quiet environment where you never had any sound at all, and all of a sudden you hear a book drops, it’s going to be very startling. The response in your cochlea is going to be larger than if you’re in a noisy environment.

Now, translate that to sensory experience. Now, you have a situation where you’re avoiding a lot of activities that produce normal sensations, painful or nonpainful. The system is then very quiet. The sensitivity is high until those things happen when you get the pain and the breakthrough pain. Lots of normal sensory input might be very important for resetting the dynamic range and “teaching” your brain that a whole range of sensations is normal and okay.

I like that example. That will help a lot of people, both practitioners and those who are in pain, realize that things are a little bit sensitized but you can desensitize them through exposure to physical therapists, to psychologists, through imagination or actual exposure-type treatments. As part of that exposure and reconciling the memory, how much of that is reconciling the emotional aspects of that environmental exposure to what’s happening?

Our emotional states are big drivers of both what we experience. How bad is that pain? For some people, the same stimulus is not a big deal. For other people, it’s tremendously bad. A lot of that emotional state comes down to appraisal, which is how you think about that stimulus, situation and your ability to cope with it. What do you think about that situation? Here’s a pain example. I was rock climbing with my five-year-old daughter and I haven’t been doing this lately, I’ve been doing a lot of other non-rock-climbing things. I did some pull-ups on the rocks and I tweaked something deep in my neck in a very strange way. When I turned my head to the right, it really hurt and I’m like, “That’s super strange. I’ve never felt anything like this before.”

HPP 102 | Neuroscience Of Nociception

When you switch from avoiding anything that might be painful to engaging and even experiencing pain as a normal part of the recovery process, the learning and plasticity in those systems that negatively alarms starts to go away.


How I respond to that and feel about it depends a lot on what means for my future. Do I think it’s going to be okay? Am I not sure? Does that mean I could become disabled, I could lose work time, or I won’t be able to do my favorite other sports? Your thoughts about the future shape the level of fear. The level of fear and those thoughts help shape what you learn from that experience. In my case, I was lucky because I immediately started turning my head. I’m like, “That hurts. It still hurts.” I spend about the next two hours doing the thing that hurt over and over again to find out what are its boundaries and I was stretching it. After a few hours, it was gone. It was interesting. It felt like the nerve pain thing. We would never know what would have happened but potentially, if I had thought, “This means I’ve done it again. I’ve done something that’s going to injure me long-term. I could have very different consequences.” Even what you learned from this movement. I moved my head, it hurt. I thought, “There’s no big deal. I’ll do it again.” If I move my head and it hurt, and if my appraisal was, “That’s bad. I’m injuring my back. I’m not going to do that ever again.” I learned something very different. Our thoughts and emotions are super important for shaping what we learned from our experience and what we take away at both conscious and unconscious levels in the brain.

I like your example because it shows you that when you become a little bit curious about your pain, instead of being aversive toward it, it starts to decrease in a lot of ways. It may not be as fast as what you experienced. For those with chronic pain, it takes a little bit longer. If you become a little bit curious and playful, you start to desensitize what can happen there. About the emotions which I think is important to what you’re saying is that when people initially hear, “Emotions are connected to my pain,” they oftentimes think that, “I have a problem with my anger. I have a problem with how I handle sadness or depression.” That’s not necessarily the case. It’s just that emotions are one part of this entire experience. You can’t necessarily just treat the emotional aspect and expect that everything else is going to get better.

I would have agreed with you because the link between emotions and pain is a mysterious one. It’s complex. Those are two very complex things interacting. We have a study that we’re doing now. The aim is to test a treatment that does focus primarily on treating the emotions. We don’t know what’s going to happen yet, but a lot of people have stories that are working for a lot of people. This is centered in part around reducing fear and letting people know that it’s okay and that pain doesn’t mean damage or hurt, in many cases.

By focusing on awareness of the fear and realizing that that’s a cause of sensitization, some people resonate with that. By focusing on that as an explanation for what’s happening, “It’s not a continuing injury in your back. It’s this sensitization which is being promoted by fear.” You can notice it and for a lot of people, that might actually help. That also goes along with as you reduce the fear, you also reduce avoidance. You engage in more normal sensory stimulation. You engage in some pain exposure. It’s not just your emotions and then that’s it. There are a number of practitioners and people who treat pain who believe that emotions like anger are important and that suppressed anger or unacknowledged anger might play a role.

I’ve heard some case studies that I find very convincing on that from people who I trust. There might be those relationships as well. Scientifically, it’s harder to explain what those relationships are, but I’ve been working with my colleague, Richard Lane. He has been writing and coming up with the theories that explain exactly that. If you have emotional experiences that you’re unable to acknowledge and process, they still live in your brain, but they’re not fully brought to light. You can’t get a conceptual handle on them. What are they? When are they going to end? What is it? There is a chance that those emotion-related brain processes might sensitize pain either as a way of keeping the emotion suppressed, so you focus on other things including somatic pain as an outlet or by other means. We have a lot more to learn about that, but I wouldn’t rule it out completely.

Some of the mindfulness practices, when you look at the research is definitely the emotional component to it. In TMS therapy, there’s a big emotional component there that people tried. John Sarno’s work was pivotal in that area and people have started to bring it to the future and study the mechanisms behind why it works. In addition to looking at the emotions and maybe why John Sarno’s work was so pivotal, what else is your lab working on as far as looking to the future of chronic pain research?

One thing I would love to do is to help explain some of these interactions between pain, cognition, appraisal, emotion, belief and then the physiological processes that go along with that. There are a lot of tantalizing stories and things that are happening to people and we want to understand how that works. That can help us bring it into a realm where it can be compared head-to-head with drug treatments, in terms of its physiological effects. By establishing physiological mechanisms, we can help to understand what are the operative principles or mechanisms and what’s happening. Psychotherapy is widely used in practice in a variety of settings, but we have a very limited understanding of what psychotherapies are doing to our brains; how our thoughts and feelings are shaped over time.

There are two prongs to the pain work that we’re doing. One prong is can we develop and push forward in developing brain-based biomarkers for pain? The goal is not to replace pain reports. The goal is to provide a solid physiological grounding for our brain targets and physiological processes that cause pain or link to pain in different individuals in different circumstances. If we test the treatment, we have some concrete physiological targets that are linked to pain. The second prong is testing those interventions. We’ve started doing a couple of chronic pain studies and testing interventions in people. We have a lot of work establishing basic mechanisms. Things like if you get social support and you have a supportive presence from your spouse, does that reduce pain? Does it affect those targets? What does it do?

HPP 102 | Neuroscience Of Nociception

As you reduce the fear, you also reduce avoidance.


Other kinds of social information whether it’s knowing what other people think or believe or even knowing that the person who’s giving you care is similar to you or have your back. All of these interpersonal factors are important in society. They’re all aspects of interventions that go beyond a particular treatment into their interpersonal interventions. They’re important clinically because of every clinical interaction between a patient and care provider, a physician or whoever involves these interactions. We’re studying how those things operate as well and what do they affect and what don’t they affect in the brain.

The social aspect of the biopsychosocial model is something that a lot of people are very interested in especially as we start to look toward things like the internet and this type of communication with patients and practitioners and how it really affects it. Tor, it’s been great talking about all your great research which is helping to inform how we understand pain. Can you tell everyone how they can learn more about you?

Let me add one more thing too, those studies of things like whether it’s a social intervention or even exercise or good sleep habits, there are so many things that can matter for people. They all rely on public money and support because it’s very unlikely that there’s going to be enough money in those kinds of free interventions, things you can do with your mind like psychotherapy. There’s not enough money in it to have major research funding the way that pharma does. We rely on people support. We rely on public funding, the National Institutes of Health and National Science Foundation, which is important because nobody else is going to make this work happen.

The best point of entry is my website, which is They can look me up on Google Scholar. I have a page there with links to a whole bunch of papers and other things. We’re launching some new projects surrounding pain. One is Pain Story. It’s going to be, which is a way to let people tell their stories in their own words about their pain experience, what’s helpful, and what’s not helpful.

I want to thank Tor for being with us and talking all about the fascinating neuroscience behind your pain and where we’re heading. Make sure to share this out with your friends and family on your favorite social media handle and hop on to iTunes and give us a five-star review, so people can access the information even faster. I want to thank all of you for being here.

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About Dr. Tor Wager, PhD

HPP 102 | Neuroscience Of NociceptionTor Wager is the director of the Cognitive and Affective Control Laboratory and Professor of Psychology and Neuroscience at the University of Colorado, Boulder. His research program focuses on the brain mechanisms underlying expectations and placebo effects, and their influences on brain systems involved in pain, emotion, and motivation. He is actively involved in the emerging field of brain-body medicine, which integrates brain activity with physiological activity in the body to promote understanding of health and disease. Dr. Wager is also actively involved in developing new analysis methods to enhance our ability to understand brain function using human neuroimaging.


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