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What studies have been done in the areas of emotional hypersensitivity and over-offendedness?

What studies have been done in the areas of emotional hypersensitivity and over-offendedness?



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It seems that emotional hypersensitivity and over-offendedness is on the rise. I've been trying to read up on it but it's hard to find scientifically backed material.

The website "Exploring your mind" has some interesting articles but I have no way of judging their accuracy. For example, The Bad Habit of Being Offended by Everything which has a link to Dealing With Hypersensitive People. While the information presented seems to make sense, it doesn't cite any authors, let alone peer reviewed papers.

What peer reviewed studies have been done in the areas of emotional hypersensitivity and over-offendedness?


The Association Between Pre-operative Pain Psychology and Hypersensitivity With Poor Functional Outcome After Knee Replacement.

To explore whether there are factors that help us to understand why some patient outcomes are not successful and identify prediction factors for progression. Assess central pain sensitisation and psychology pre- and post-surgery with reliable tools that explore prediction tools for good/poor progression and improve patient selection, patient preparation and timing for surgery.

The aim of this project is to explore the effects of pre-surgical central pain sensitisation on pain and function outcomes post-TKA. Central pain sensitisation will be assessed using pressure algometry and the Pain Catastrophizing Scale will be used to explore pain psychology. Functional outcomes post-TKA will be assessed using a commonly used scale for patients' self-reported outcomes (Oxford Knee Score), visual analogue scale, a star excursion balance test and four recommended patient performance-based tests.


Condition or disease Intervention/treatment
Outcome After Total Knee Arthroplasty Procedure: total knee arthroplasty

Knee osteoarthritis (OA) is a major cause of disability around the world it is the most common chronic condition in primary care in the UK. By 2030 it is predicted to be the greatest cause of disability in the general population. An effective end-stage treatment for knee OA is knee-replacement surgery, which was first done in the 1970s and 1980s.

In England and Wales, the number of knee-replacement procedures recorded by the National Joint Registry in 2013 was 91,703, which represents an increase of 0.9 % over 2012. The data analysis by the National Joint Registry and the Office of National Statistics suggests that, by 2030, primary TKAs will increase by 117% from the 2012 level. Subsequently, TKA revision surgeries are expected to increase incrementally by 332%. There is a similar estimation of demand for revision TKA surgeries in the United States by 2030, they are expected to rise by 601% from the 2005 level. The United States estimation of primary TKA is for growth of 673% from the 2005 level, which is similar to England and Wales's upper-limit projections.

Post-TKA, 75-85% of patients report satisfaction with surgery outcomes, while the remaining 15-25% are dissatisfied . Total knee arthroplasty's success has traditionally been evaluated from the surgeon's perspective, e.g. the presence of surgical complications or implant survival. This is gradually changing to involve the patient in measuring health outcomes and decision-making processes. Patient-reported outcome measures (PROMs) have evolved to explore patient perspectives by monitoring the quality of care in health organizations and conducting clinical trial outcomes.

Worldwide National Joint Registry summarise the common indication for TKA revision are 29.8% due to aseptic loosening, 14.8% infection and 9.5% due to pain. Most prediction studies show that pain and psychology pre-operation may predict poor outcomes post-TKA. A systematic review by concludes that pain catastrophizing predicts chronic pain post-TKA. Pain catastrophizing is defined as a construct that reflects anxious preoccupation with pain, an inability to inhibit pain-related fears, amplification of the significance of pain vis-à-vis health implications, and a sense of helplessness regarding pain.

Chronic post-surgery pain is significantly associated with preoperational central sensitisation as in post-shoulder subacrominal decompression and hernia repair. Regarding post-TKA, a study by Lundblad et al. (2008) concluded that the preoperational hand electrical pain threshold significantly predicts pain outcomes one year post-TKA. The study explored the association between chronic pain post-TKA and preoperation widespread pain sensitisation using pressure algometry. Both study association without control the psychological confiding factor. The correlation with Western Ontario and McMaster Universities Osteoarthritis Index pain score (WOMAC) is questionable due to weakness of WOMAC with post TKA population such as low sensitivity of WOMAC's stiffness subscale reduces the overall standardized response mean and high ceiling effect Psychological pain thinking is assessed using the most widely used measuring scale: Pain Catastrophizing Scale (PCS). PCS assesses pain thinking in three dimensions: rumination ("I can't stop thinking about how much it hurts"), magnification ("I worry that something serious may happen") and helplessness ("It's awful and I feel that it overwhelms me").

The current study will investigate preoperational central sensitisation using pressure algometry, in addition to the Pain Catastrophizing Scale (PCS), to explore psychological factors. There may be some correlation between preoperational central sensitisation and post-TKA outcomes such as pain and functional improvements.

To the best of our knowledge, no previous study has explored central sensitisation using pressure algometry and the Pain Catastrophizing Scale and possible correlation with its effects on pain and function recovery post-TKA. Pain and function can be accurately assessed before and after TKA using visual analogue scale, Oxford Knee Score, balance and performance functional tests. No previous study has correlated preoperational central sensitisation and pain psychology post-TKA on the Oxford Knee Scale as commonly used patients' self-reported outcome measures.

Thus, the study may explore accurate and objective prediction factors of post-total-knee arthroplasty progression. Potentially, reliable outcome prediction could, however, improve patient selection for surgery, as appropriate timing for surgery depends on patient symptoms and efficient patient preparation for surgery if it is to be cost-effective. Accurate preoperative prediction is crucial to minimize the potential for unrealistic expectations.

Layout table for study information
Study Type : Observational
Estimated Enrollment : 50 participants
Observational Model: Cohort
Time Perspective: Prospective
Official Title: The Association Between Pre-operative Pain Psychology and Hypersensitivity With Poor Functional Outcome After Knee Replacement
Estimated Study Start Date : September 12, 2020
Estimated Primary Completion Date : February 1, 2022
Estimated Study Completion Date : December 1, 2022

Resource links provided by the National Library of Medicine

Anxiety in Children and Adolescents with Autism Spectrum Disorders

Anxiety and poor stress management are common concerns in clinical samples of children with autism spectrum disorders (ASD). Anxiety may worsen during adolescence, as young people face an increasingly complex social milieu and often become more aware of their differences and interpersonal difficulties. This review summarizes the state of research on the prevalence, phenomenology, and treatment of anxiety in youth with autism and related conditions such as Asperger’s disorder. Using search words autism, asperger(s), or pervasive developmental disorder and anxiety or anxious to find reports published between 1990 and 2008, this review identified 40 papers. The results of the review suggest that anxiety, whether measured categorically or dimensionally, is indeed common in children and adolescents with autism spectrum disorders and may be a source of additional morbidity. The assessment of anxiety disorders in ASD should be conducted using multiple informants and modalities, as children with ASD often do not display age-typical symptoms of anxiety. To date, relatively few controlled intervention studies using well-characterized samples have been conducted despite preliminary evidence for efficacy of select pharmacological and psychosocial approaches. Recommendations for future applied research are presented and clinical implications are explored.

Autism spectrum disorders (ASD) are characterized by deficits in social interaction and communication, as well as the presence of stereotyped behavior and restricted interests (American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders 4 th Ed. -Text Revision, 2000). Once regarded as rare, this group of disorders - which includes Autistic Disorder, Asperger’s Disorder, and Pervasive Developmental Disorder-Not Otherwise Specified (PDD-NOS), has received a great deal of professional and scientific attention. Based on recent survey findings, the United States Centers for Disease Control (2007) reported that ASD may be as common as 1 in every 152 children suggesting that these disorders pose 𠇊n urgent public health issue.”

The reasons for the increase in the estimated prevalence over the past decades are not entirely clear, but several possibilities can be advanced to at least partially explain these increased rates. First, the early studies on prevalence relied on clinically identified cases rather than community-based surveys. Cases not in treatment were therefore missed moreover, only the most severe cases were likely recorded. Second, even those studies that conducted community surveys used narrow case definitions. By contrast, more recent studies have used broader diagnostic criteria and better sampling methods, thus identifying more cases. Finally, recent studies have used better diagnostic instruments, which has served to improve differential diagnosis among the different spectrum disorders as well as helped to delineate ASD from other psychiatric disorders in children (Chakrabarti & Fombonne, 2005). As more children with ASD are identified, there will likely be a rise in the number of children and families seeking treatment. Regardless of the cause(s) accounting for the higher prevalence estimates, therefore, clinicians are now faced with increasing numbers of children and teenagers with ASD, and their families, who require assessment and effective treatment.

In the clinical setting, anxiety-related concerns are among the most common presenting problems for school-age children and adolescents with ASD (Ghaziuddin, 2002). Recognition of anxiety problems in this population is not new. Indeed, in his original description of children with 𠇌lassic” autism, Kanner (1943) noted that a number of them had substantial anxiety problems. However, the evaluation and treatment of anxiety in this population has only recently received the empirical attention it deserves. There is an urgent need for the development of effective approaches to assess and treat children and adolescents with ASD (Lord et al., 2005), including treatments addressing associated problems such as anxiety.

Currently, anxiety is not considered a phenomenological characteristic of ASD. Although it is often assumed that individuals with ASD prefer isolation and low social contact, many people with ASD are intensely aware of their social disconnectedness and appear to wish it could somehow be different (Attwood, 2000). It is logical to conjecture that the social disability associated with ASD could engender anxiety – especially in higher functioning youth who have an awareness of their social disability. If a child has a co-occurring anxiety disorder, it could compound the overall social impairment associated with ASD. For example, social anxiety may contribute to avoidance of social situations, awkward interactions with peers, and promote further isolation from same-age peers (Myles, Barnhill, Hagiwara, Griswold, & Simpson, 2001). Thus, anxiety may have bidirectional effects with the social disabilities of ASD. For these reasons, a developmental approach to understanding how anxiety develops, and how it may interact with the core disabilities of ASD, is important. This is also relevant clinically in as much as very high functioning adolescents with milder forms of ASD may present for clinical concerns due to anxiety, as opposed to the ASD per se.

An empirically based understanding of anxiety in children and adolescents with ASD is necessary to inform accurate assessment, case conceptualization, and treatment planning. To that end, this review summarizes research on anxiety in children and adolescents diagnosed with ASD. The specific aims are: (1) to summarize the empirical research on the prevalence, presentation, and treatment of anxiety in school-age children and adolescents with ASD (2) to offer guidance on the ‘next steps’ for clinical research in this area and (3) to provide clinical recommendations based on our understanding of anxiety in this population.


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

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.

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.”

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?

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 Wagerlab.Colorado.edu. 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 PainStory.science, 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.

Important Links:

    – previous episode – previous episode – Dr. Tor Wager
  • Healing Pain Podcast on iTunes
  • www.DrJoeTatta.com/102Download

About Dr. Tor Wager, PhD

Tor 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.

The Healing Pain Podcast features expert interviews and serves as:

A community for both practitioners and seekers of health.
A free resource describing the least invasive, non-pharmacologic methods to heal pain.
A resource for safe alternatives to long-term opioid use and addiction.
A catalyst to broaden the conversation around pain emphasizing biopsychosocial treatments.
A platform to discuss pain treatment, research and advocacy.


What is complicated grief?

As a general rule, when we face a loss we go through a series of stages that help us to overcome the grief. We go from a first phase of denial that allows us to soften the pain of the news, to experience great anger at the loss and sink into the deepest sadness to finally come to acceptance.

In complicated griefs, we don’t go through all these stages, we get stuck in one of them, so we don’t end up accepting the loss. Our inner world is not restructured to accept reality because we cannot get rid of recurring thoughts about the person who left us, which prevents us from getting back to life.


AQA Psychology A Level Addiction

if it is not fully functioning, the nicotine stays around longer and there is more dopamine.

application: nicotine replacement therapy, which will have good implications for economy (NHS deal with less of the bad health effects that comes with cigarettes) and people are helped. However, the biological explanation takes the responsibility away from people

reductionist- which has lead to treatments but also ignores many other factors

individual differences- the other risk factors

ignores cognitive aspects (dysfunctional cognition)

Research support- Levin et al, Carter and Tiffany

dependent smokers reacted strongly to cues presented to them, reporting higher levels of craving.

scientific- the studies done are lab studies (skinner)

Practical applications- people avoid cues

Negative implications- Gambling places may make sure they encourage addiction

Other explanations- SLT to why people start it, cognitive aspects

To measure the participants objective skill levels, Griffiths recorded the gamblers behaviour. The experimenter stood nearby recording the amount of time spent there, and how much money was won

They said their their thoughts aloud while gambling

participants were then interviewed and said how much skill they thought that had


Introduction

In a recent theoretical review, Smith et al. (2018) eloquently describe a model outlining the ways in which emotional experiences unfold and reach awareness. This process begins with one’s affective response—i.e., the coordinated changes that occur in one’s body and cognitive or attentional state, in response to a particular situation. Affective responses can be triggered in a bottom–up fashion or alternatively by forming or reactivating perceptual representations of current, past, or imagined situations and appraising their novelty, relevance to one’s goals or values, and controllability. Cognitive and attentional habits can bias the formation of both perceptual and appraisal-based representations, and bottom–up and top𠄽own factors can shape higher-order representations of the affective response and its probable meaning.

Smith et al. (2018) go on to argue that the representations we form of the situation and our subsequent response to it can be “selected” for and actively maintained in working memory. Activating a perceptual representation of an affective response allows one to consciously experience the change in body-state that has occurred, whereas activating a conceptual representation of that response allows one to consciously recognize and describe the emotion that one is feeling (or the emotion of another person whose affective response has been simulated). Top𠄽own influences determine which (if any) of the representations formed reach conscious awareness.

The ability to generate and experience emotions is clearly evolutionarily advantageous, as they motivate us to respond in ways that can help us meet our needs. However, learning to regulate emotions is also important. According to Gross (1998a,b, 2015), adults use five main strategies (alone or in combination) to manage their emotions. Situation selection involves actively approaching or avoiding stimuli or situations that are expected to trigger particular affective responses. The remaining strategies involve top𠄽own control. People can physically alter the external environment in ways that make it easier for them to function well (situation modification). They can also use attentional deployment by shifting one’s external focus (using selective attention), or by shifting attention to calming internal thoughts or mental images (engaging working memory), one can reduce the likelihood that affective responses that make one uncomfortable will reach conscious awareness. An individual might also make a cognitive change for example, they might use verbal reasoning or reappraisal to change how they interpret an affective response. Finally, one can engage in response modulation (e.g., expressive suppression).

The models proposed by Gross (1998b) and Smith et al. (2018) can explain why our emotional experiences and our ability to self-regulate vary over time. Importantly, however, they may also help to explain individual differences in stable traits such as alexithymia. This trait, seen in approximately 10% of the general population (Mattila et al., 2010), is characterized by difficulties identifying feelings (DIF), difficulties describing feelings (DDF), an externally oriented thinking style (EOT), an impoverished fantasy life, and problems distinguishing between emotional arousal and somatic sensations (Nemiah et al., 1976). Smith et al. (2018) suggest that individuals scoring high (vs. low) on alexithymia may: (a) generate fewer or more poorly differentiated affective responses (b) perceive/represent their affective responses in a concrete or coarse-grained manner and/or (c) have developed a set of stable cognitive habits that make it difficult for them to exercise the top𠄽own cognitive control that is required for them to consciously experience their affective responses and the emotions that they are feeling. Problems in any or all of these areas would make it difficult for them to identify and describe their emotions, and this, in turn, could limit their ability to understand and regulate them.

In the present study, we explored the idea that alexithymia is associated with atypicalities in a range of bottom–up and top𠄽own processes that impact how affective responses are generated, experienced, and regulated. To do this, we collected data from a large sample of university students regarding how they process and respond to a range of body-based and environmental sensory cues and the extent to which they engage in processes not driven by environmental stimulation, such as visual imagery, dreaming, and some aspects of problem-solving. We then examined interrelationships between these measures using a variety of approaches. The first set of analyses were undertaken to examine general patterns seen in the sample as a whole. The second set of analyses explored the possibility that patterns of association between variables might differ across distinct subgroups of individuals.

Our study builds on past research suggesting that alexithymia is linked to atypicalities in sensory processing that could impact emotional embodiment. Much of the recent work in this area has focused on the ability to perceive internal body sensations correctly (interoceptive accuracy or IA). Based on their meta-analysis, Trevisan et al. (2019) concluded that there is a moderate, negative association between alexithymia and self-reported IA. Based on its links with performance on objective tests of IA, Murphy et al. (2018) argue that alexithymia may serve as an index of “multidimensional, multi-domain, interoceptive impairment” (p. 405).

Although interoceptive inputs undoubtedly contribute to embodied feelings, they cannot be the only factors that drive them, given that individuals experiencing pure autonomic failure still experience these states (Heims et al., 2004). On these grounds, we might expect alexithymia to be associated with atypicalities in the processing of a range of sensory cues. Research generally supports this idea, although the direction of effects is mixed, with some studies linking alexithymia to exaggerated neural, physiological, or behavioral responses to exteroceptive or body-based cues (e.g., Sivik, 1993 Nyklicek and Vingerhoets, 2000 Schafer et al., 2007 Bogdanov et al., 2013) and others linking it to reduced responsiveness (e.g., Pollatos et al., 2008 Goerlich-Dobre et al., 2014b Gaigg et al., 2018). Alexithymia is also associated with atypicalities in multisensory integration, although the direction of the effects has varied (see Miles et al., 2011 Thakkar et al., 2011 Cascio et al., 2012 Germine et al., 2013 Grynberg and Pollatos, 2015 Georgiou et al., 2016). The mixed results from studies in this area could reflect the fact that researchers have not typically considered in their study designs the possibility that there may be subtypes of individuals with alexithymia who generate, experience, and regulate their emotions in different ways. Exploring this possibility is important for advancing theory and research in alexithymia.

Several studies have used the 20-item Toronto Alexithymia Scale (TAS-20 Bagby et al., 1994) in combination with other measures to look for evidence of subtypes of alexithymia. Lane et al. (2015a) distinguished anomic and agnosic forms—the former being associated with problems naming emotions but intact theory of mind and the latter with problems forming conceptual representations of emotions and impaired theory of mind. In contrast, Kajanoja et al. (2017) identified a subtype characterized by strong DIF and symptoms of depression and anxiety and another characterized by elevated DDF and EOT scores and impaired empathy.

Other subtyping studies have used the Bermond Vorst Alexithymia Scale (BVAQ Vorst and Bermond, 2001), which samples both cognitive traits (the ability to identify, verbalize, and analyze one’s emotions) and affective traits (flattened affect and impoverished fantasy) that are associated with alexithymia. By applying factor analysis and principal component analyses to BVAQ scores, Bermond et al. (2007) identified a subtype characterized by high scores on both cognitive and affective dimensions (type I) and another characterized by high scores on the cognitive dimension but typical or unusually low scores on the affective dimension (type II). Although consensus is not universal (Bagby et al., 2009), most subtyping work using the BVAQ recognizes at least these two variants (e.g., Vorst and Bermond, 2001 Larsen et al., 2003 Berthoz and Hill, 2005 Goerlich-Dobre et al., 2014a). Some researchers describe a third subtype (type III) characterized by high scores on the affective dimension only (Bermond et al., 2006). Moormann et al. (2008) also recognized a lexithymic subtype (who score low on both dimensions), a modal subtype (who score in the average range on both dimensions), and a mixed class that does not fit into any category. They point out that because those with type III, lexithymic, and modal profiles do not have problems with emotional understanding and generally have good psychological health, it may be misleading to refer to them as alexithymia types.

Subtyping work using the BVAQ has been fruitful however, the distinctiveness between the cognitive and affective dimensions is not always clear indeed, there is overlap between these dimensions, particularly with regard to the 𠇊nalyzing” subscale, which taps into EOT (de Vroege et al., 2018). Preece et al. (2017) also described several limitations with the BVAQ’s 𠇎motionalizing” subscale (see also Watters et al., 2016). Another issue concerning BVAQ studies that have compared different subtypes with regard to their neural substrates (Goerlich-Dobre et al., 2015) and patterns of autonomic reactivity (Bermond et al., 2010) is that they have relied on median split procedures to create groups. The use of latent profile analysis (LPA) may be preferable, as it allows one to categorize participants in a heterogeneous sample into more homogenous subgroups based on their responses to continuous variables (Berlin et al., 2014).

In the present study, we took a unique approach to explore individual differences in alexithymia expression. Our approach was motivated by the idea (expressed by Smith et al., 2018) that two key factors contribute to the development of individual differences in people’s emotional awareness: (a) genetic/epigenetic factors and personality traits with an innate component and (b) learning, through which cognitive habits are established. The idea that differences in these factors might result in individual differences in alexithymia led us to explore links between alexithymia and sensory processing sensitivity (SPS). SPS is a genetically predetermined trait, and its expression varies as a function of life experiences (Aron et al., 2012). SPS is characterized (in part) by a tendency to become easily overwhelmed by environmental stimuli and multitasking demands and by increased sensitivity to subtle and aesthetic features of one’s environment (Aron et al., 2012). The former feature of SPS is positively associated with DIF/DDF, and the latter is negatively related to EOT (Liss et al., 2008 Rigby et al., 2020). Unlike many people with alexithymia, individuals scoring high on SPS have a “rich” inner life, which might suggest an enhanced ability to keep perceptual representations of past, current, or imagined situations active in working memory. To our knowledge, no one has explored how/if two additional features of SPS—the tendency to process information at a deep/complex level and to approach novel situations cautiously—may relate to alexithymia. Doing so is of interest, as all of the features of SPS could impact how affective responses are generated, experienced, and regulated. Indeed, in adults, all three aspects of SPS are positively associated with neuroticism and negative affectivity (Lionetti et al., 2019).

Whether or not they have SPS, individuals vary in the ways in which they typically process and regulate their responses to sensory information in daily life. Given this, we were also interested in exploring how one’s sensory processing style might impact the expression of alexithymia. Dunn (1997) has characterized trait sensory processing styles along two dimensions: neurological threshold and behavioral regulation. The former describes the amount of sensory information required to activate the central nervous system, and the latter specifies whether an individual typically responds to sensory information actively or passively. Hyposensitivity to certain kinds of stimulation may lead to a passive failure to respond (low registration or LR) or to attempts to actively seek out stimulation (sensation seeking or Seek), whereas hypersensitivity may cause one to become easily overwhelmed (sensory sensitivity or Sen) or to actively try to avoid or reduce exposure to stimulation (sensory avoidance or SA). An individual’s sensory processing style is reflected in the relative strength of their Seek, SA, LR, and Sen tendencies, which can be assessed via a self-report measure called the Adolescent/Adult Sensory Profile (AASP Brown and Dunn, 2002).

Relationships between alexithymic traits and AASP scores have been examined indirectly in several studies involving clinical populations. Co-occurring alexithymia has been shown to predict elevated scores on LR in adolescents with autism spectrum disorder (Milosavljevic et al., 2016). Bashapoor et al. (2015) observed that men with substance dependence showed heightened DIF and DDF, and elevated scores on LR, Seek, and SA, relative to a control group. Serafini et al. (2017) found that DIF and DDF scores were positively correlated with LR and that TAS-20 Total scores were positively associated with LR, Sen, and SA in adults diagnosed with a major mood disorder. Finally, Serafini et al. (2016) showed that AASP scores mediated the relationship between alexithymic traits and quality of life in participants with mood disorders. Although these findings suggest that alexithymia is linked to particular ways of processing and regulating one’s responses to sensory information, to our knowledge, no work has examined relationships between alexithymia and individual AASP scores (or patterns across these scores) in non-clinical samples.

In light of the discussion earlier, our first main objective was to examine interrelationships between alexithymia, SPS, and sensory processing styles in a non-clinical sample of young adults. In Part A later, we addressed three key questions: (1) “What are the relationships between alexithymia, SPS, and IA?” (2) 𠇍o any features of SPS improve prediction of alexithymia above and beyond that accounted for by IA?” and (3) 𠇍o sensory processing styles mediate the relationship between IA and specific alexithymic traits?” We expected to replicate past work demonstrating links between alexithymia and aspects of sensory processing beyond those supporting IA, but our approach allowed us to extend previous findings by considering multiple measures of sensory processing simultaneously.

Our second main objective was to test the novel prediction that subtypes of alexithymia could be distinguished based, in part, on aspects of sensory processing. Given the current interest in exploring links between alexithymia and IA (e.g., Brewer et al., 2016) and our own interest in studying aspects of one’s sensory processing style more generally, we included scores on the TAS-20 subscales, a measure of IA, and the AASP as input variables in an LPA. This analysis, described in Part B, allowed us to address two key questions: (1) �n subtypes of individuals be identified based on their alexithymic traits, IA, and sensory processing styles?” and, if so, (2) “How do the observed subclasses differ with regard to their latent profiles?” We expected to find that individuals could be distinguished by the relative strength of different alexithymic traits and by differences in IA and sensory processing styles. We also performed planned contrasts comparing the observed classes on measures of SPS. Finally, we examined how each of the classes scored on measures of depression, anxiety, and stress, as high scores on these measures might indicate problems with emotion regulation.


References

Brydon, L., Walker, C., Wawrzyniak, A., Chart, H., & Steptoe, A. (2009). Dispositional optimism and stress-induced changes in immunity and negative mood. Brain, Behavior, and Immunity, 23, 810-816.

Gray, J. D., & McEwen, B. (2013). Lithium’s role in neural plasticity and its implications for mood disorders. Acta Psychiatric Scandinavica, 128, 347-361.

Osdoba, K., Mann, T., Redden, J., & Vickers, Z. (2015). Using food to reduce stress: Effects of choosing meal components and preparing a meal. Food Quality and Preference, 39, 241-250.

Saito, Y., & Tada, H. (2007). Effect of color images on stress reduction: Using images as mood stimulants. Japan Journal of Nursing Science, 4, 13-20.

Sherman, G., Lee, J., Cuddy, A., Renshon, J., Oveis, C., Gross, J., & Lerner, J. (2012). Leadership is associated with lower levels of stress. Proceedings of the National Academy of Sciences, 19(44). doi: 10.1073/pnas.1207042109.

Stough, C., Scholey, A., Lloyd, J., Spong, J., Myers, M., & Downey, l. (2011). The effect of 90 day administration of a high dose vitamin B—complex on work stress. Human psychopharmacology, 26, 470-476.


Roughly one-fifth of all adults with ADHD have tried cognitive behavioral therapy (CBT) and/or ADHD coaching — two popular natural treatments receiving ratings of ‘extremely effective’ or ‘very effective’ by 41% and 48% of ADDitude readers, respectively. 1 Still, some confusion persists.

CBT is a short-term, goal-oriented form of psychotherapy that aims to change negative patterns of thinking and change the way patients feels about themselves, their abilities, and their future. CBT is supported by clinical evidence and research results showing that the therapy delivers real-world benefits for adults with ADHD — namely higher self-esteem, productivity, and happiness.

ADHD coaching is an ongoing collaborative partnership created to facilitate greater self-awareness, self-regulation, and self-initiative for clients with ADHD. It is built upon unconditional acceptance and a powerful appreciation of the client’s potential, uniqueness, strengths, capabilities, and wholeness. ADHD coaches are well-versed in ADHD-specific coaching competencies. The coaching process empowers clients to accomplish personal and professional goals with customized strategies built specifically for ADHD minds.

In the recent ADHD Experts webinar “How CBT and ADHD Coaching Help Adults Manage Their Symptoms Naturally,” Dr. Russell Ramsay and David Giwerc highlighted the differences between CBT and ADHD coaching, and explained how each ADHD therapy helps mitigate symptoms of ADHD. Below, they answer some of the most common questions from ADDitude readers.

1.Where can I find accredited practitioners of both CBT and ADHD coaching?

ADHD Coaching

The following are recommended resources for finding experienced CBT practitioners:

2. Aside from checking accreditation, what should patients with ADHD look for and ask when assessing whether an ADHD coach or CBT practitioner is a good fit for them?

ADHD Coaching

The relationship between coach and client is a partnership a good fit is vital. This article presents a list of questions to ask a prospective ADHD coach. In the responses, listen for less tangible, but equally important characteristics such as style, energy, and tone from each prospective coach. This guide from the ADDCA Blog can help provide additional guidance.

I’d recommend asking about their experience working with adults with ADHD, including diagnostic evaluations and follow-up therapy. Ask about the CBT manuals or other books with which they are familiar, and their view on the executive function model of ADHD. This will also be a way to get a sense of “fit,” though that can be a different matter.

3. ADHD coaching services are often available via Zoom or other video platforms. Is the same true for CBT? Do practitioners typically accept and begin treating new patients digitally?

It depends on the state, but most are allowing cross-state services by licensed psychologists, or have made it easy to obtain a temporary license. This will likely persist after restrictions due to COVID, at least within states. There is a consortium of states through PsyPACT that will credential therapists to provide remote services across state lines for those participating states.

4. How young can an individual begin and benefit from ADHD coaching and/or CBT? Are these treatments appropriate for teens? Is it possible to be too old to benefit from ADHD coaching and/or CBT?

ADHD Coaching

Coaching is appropriate for children, adolescents, young adults, and adults. Chorological age is not a criterion for coaching it is the age level of the individual’s neurological functioning that is important. An 18-year-old may have the executive functions of a 13-year-old. A well-trained ADHD coach will support a client based on the age level of executive functioning exhibited during coaching.

Teen coaching, for example, requires customized education that is incorporated into the session in an engaging way. A teen may need to focus on a specific task, sustain their focus, and associate it with something that helps them understand it. For the teen to make progress, parents need to be educated about their child’s type of ADHD and their child’s weaknesses and strengths.

ADD Coach Academy has an accredited family training program dedicated to teaching ADHD coaches the dynamics of the family and how to best work with children of different ages who have ADHD. Coaches are only eligible for family training after they have completed the key requirements for ADHD basic coach training or ADHD advanced coach training.

ADHD coaching can also be very effective for older individuals, who are wiser in terms of experience and context. One difference may be that an older person with ADHD may need more time to access information from their long-term and working memory. A good ADHD coach would bear this in mind and provide more space and time for the older client to process and articulate their responses when questioned.

Though CBT is largely used with adults, there are some initial studies of the adult ADHD CBT approaches being “down-fitted” for older teens with ADHD. There are some CBT approaches specific to school and driving designed specifically for teens. High school-age teens with ADHD could benefit from CBT, though their receptiveness will likely be an issue.

One does not age out of CBT for adult ADHD. In fact, seniors with ADHD are a growing group, though no specialized protocols exists yet. Kathleen Nadeau, Ph.D., is currently working on a book on seniors with ADHD – her content on ADDitude might provide additional information.

5. What would you recommend for children with ADHD who struggle with executive functions, negative thinking patterns, etc.?

ADD Coaching

Working with children and their families may be the biggest segment of ADHD coaching with the largest demand. In fact, ADDCA created a specialty family training program that focuses on the dynamics of the family.

So long as children are able to communicate and be engaged in a structured but flexible coaching conversation, coaches with family training work with young children adolescents, teens college aged and young adults.

For elementary school children, parent and teacher training are still the preferred approaches. There are some CBT approaches modified for children to help with thought patterns and behaviors — for example, the past work of Phil Kendall. Richard Gallagher, Howard Abikoff, and colleagues also have a wonderful program for building organizational skills in children. The Smart But Scattered (#CommissionsEarned) series also offers a wonderful approach for executive functions, not limited to ADHD.

6. Does ADHD coaching exist for parents to teach them ways to better communicate with and guide their young children with ADHD? (Or is behavioral parent training the more appropriate choice here?)

An ADHD coach will work with parents to identify ways to communicate with their children that encourages growth, curiosity, and confidence. ADHD coaches help parents become aware of what will positively activate their child’s brain and reinforce what they can do using their strengths. The parents also must be aware of the natural sources of motivation for their child.

7. Is it necessary to have a formal ADHD diagnosis before pursuing coaching and/or CBT?

ADHD Coaching

Yes, a formal assessment or evaluation with a health care practitioner who specializes in the diagnosis and treatment of ADHD and co-occurring conditions is a vital component of effective comprehensive treatment of ADHD.

ADHD coaching is an integral component of comprehensive treatment. However, ADHD coaches are not diagnosticians. Coaching can bridge the gap between biology and behavior, but it is not the only answer. Effective treatment often includes an ADHD psychiatrist, a CBT therapist who is experienced with ADHD, and a well-trained ADHD coach.

When a coaching client is frustrated by their ability to function in specific situations, tasks, and environments, then I refer them to an MD specializing in the diagnosis and treatment of ADHD or a therapist who is experienced with the diagnostic process for ADHD and co-occurring conditions. The doctor can help the patient receive a proper diagnosis, which unlocks targeted medication at a correct dosage. Research tells us that, in 80 percent of cases of ADHD, treatment with stimulants will mitigate the impairing symptoms of ADHD. Even then, the pill does not give you the skill. But it may put a client on a level playing field to pay attention and sustain focus so they can work with a coach.

CBT focuses on problems and solutions, so even if someone does not meet diagnostic criteria for ADHD but struggles with executive functions (EF), they could likely benefit from the CBT approach for ADHD. That said, some sort of initial interview is good practice in order to determine what is causing the EF difficulties, such as an adjustment to school/work, or mood or anxiety issues, as some modification of treatment might be indicated.

8. With a diagnosis, do some insurance plans cover the cost of CBT and/or coaching for ADHD symptoms?

Most insurance plans do not cover ADHD coaching. Clients pay out of pocket. In rare cases where they do pay, Insurance companies will limit the number of sessions. This does not allow for adequate sessions to support clients. Plus, it disrupts the client’s momentum especially when they are experiencing success. ADHD coaching requires more time than life coaching to get through the invisible barriers impeding the client’s ability to create progress in different areas of their life.

9. Can you offer some guidance re: reasonable costs for CBT and ADHD coaching services? (Cost appears to be a formidable and common barrier to treatment for many people in attendance today.)

ADHD Coaching

As a general guide, ADHD coaching costs about the same as therapy or life coaching. One-hour sessions may range in price from $75 to $250, and sometimes more. There are many variables that impact the costs of coaching. The question that needs to be asked is this: How much is coaching improving the quality of my life or my child’s worth? If coaching can dramatically improve satisfaction, fulfillment, contribution, and productivity in the world, what would I be willing to pay? Costs must be addressed with each coach being considered because the cost of ADHD coaching varies.

  • There are ways to reduce the costs for ADHD coaching services. A growing number of coaches are offering a sliding-scale fee based on your level of financial comfort or a percentage of your annual income. When interviewing, ask the coach about possible alternatives to their full fee. Sometimes, if the coach and potential client have a strong connection, they might be willing to work with you.
  • If you are seeking coaching in the workplace to improve your performance or prepare for a new role, you can approach your Human Resources department and request reimbursement for the full fee or a portion of the fee. However, by doing this you are informing your company about your ADHD diagnosis. Many adults choose not to do this due to negative perceptions associated with the disorder.

Pricing for CBT depends on where one lives, private practice vs. clinic-based therapists, etc. The Penn Psychiatry Adult ADHD Program has reduced fees for trainee clinicians. Clinical psychology graduate programs often offer reduced fees for supervised graduate therapists, though it depends on the program for CBT and/or ADHD services.

10. What are some reasonable metrics for success? How can we tell if the coaching or CBT is working the way it should?

ADHD Coaching

The ADD Coach Academy participated in a study assessing the benefits of ADHD coaching for college students. The metrics of success we looked at were improvements on measures of self-efficacy, knowledge of personal learning style, and measures of self-control. Reduced procrastination, consistent completion of goals, and increased confidence in strengths were some of the observable outcomes.

What are your behavioral goals for CBT and are you meeting those goals for change? Follow-up scores on symptom and EF measures gathered during the initial evaluation can also be reviewed to assess change. Also, ask someone who lives with the patient if he or she notices a difference.

11. Can you explain the differences between CBT and DBT?

Both fall under the CBT umbrella. DBT emerged as the treatment of choice for Borderline Personality Disorder and focuses on emotional regulation and tolerating and managing emotional dysregulation, often accompanied by self-harming and suicidal behaviors. DBT comprises different coping modules that also address setting limits, asking for help, and modifying interpretations (thoughts) about feelings. DBT has been modified for adult ADHD by Alexandra Philipsen in Germany, developing coping modules geared for adult ADHD rather than the main focus on emotional dysregulation.

Acceptance and Commitment Therapy or ACT is another such “third wave” of behavioral therapies that emphasizes the ability to accept and tolerate emotional discomfort and negative thoughts without necessarily changing them as a precondition for engaging in (committing to) valued actions.

12. How long has CBT been used to treat ADHD? How ‘new’ is it, really?

The first outcome study (a chart review) of CBT for adult ADHD was published in 1999 by a Harvard group. Our program started in 1999, so it has been little over 20 years that it has been used in practice, but the past decade has seen a geometric progression of outcome studies in support of its use.

1 Frye, Davon Rodgers, Anni Layne. Special Report: How You Are Treating ADHD or ADD Today. ADDitude Magazine (2017). https://www.additudemag.com/adhd-treatment-options-caregivers-adults-survey-results/

SUPPORT ADDITUDE
Thank you for reading ADDitude. To support our mission of providing ADHD education and support, please consider subscribing. Your readership and support help make our content and outreach possible. Thank you.


What I wanted to learn by exploring the topic/issue/disability/learning difference further

I wanted to have a deep understanding of ADHD so that I could be able to explain a number of problems with a child’s and in some cases, an adult’s intellectual, social, and psychological development (Lopez – Vergara & Colder, 2013). I was keen on finding out how behavior ends up affecting these factors in the development of a person. I wanted to see how the integration of medication and therapy in the field of healthcare and education plays a role in assisting individuals with ADHD cope with their living environment. At the same time, I wanted to learn the current situation and the emerging trends that are affecting the field of study and practice of teaching special education, with an emphasis on the effects of any present strategy on the development of a person with ADHD.

I understand that being hypersensitive is not a disorder by itself. Thus, my inquiry into this topic was mainly because this characteristic of a person occurs within another topic of attention deficit that is considered a disorder. Thus, I wanted to know how hypersensitivity and attention deficit occur and influence each other in a person’s character. Knowing this would allow me to make sense of the developments in education concerning special education, which is going to be part of my career.

Hypersensitivity is a wide topic with a variety of applicable knowledge. In this regard, it can be too confusing to work with the entire scope of hypersensitivity. Therefore, having sufficient knowledge of the topic and any related concept would allow me to narrow down to a niche of the subject, which can then serve as my basis for specializing when I am in my professional practice. It will also be a good thing to do for my additional learning needs.

After learning about hypersensitivity as a characteristic of attention deficit disorder, I wanted also to understand other characteristics of the condition. This would provide me with an all-round capacity to handle personal and organizational queries on the matter. It would also enable me to provide a convincing rationale for my career goals. Knowledge of these concepts and their prevalence in society will make me a better practitioner, and that is why I opted to explore this hypersensitivity topic further.

Further exploration urges also emerged after finding out the basic characteristics of hyperactivity like fidgeting, talking nonstop, being constantly in motion, and having difficulty in doing quite tasks and activities (Lopez – Vergara & Colder, 2013). These are also characteristics of other medical and non-medical conditions. Therefore, it is helpful to know how to identify and differentiate them to avoid misinterpretations. Correct recognition will make intervention easier. In this case, I was considering intervention in education and health care. Besides that, I have been interacting with a number of research reports and general scholarly texts on the matter.

For example, research by Park et al. (2011), sought to find out the prevalence, correlates, and comorbidities of ADHD symptoms in a Korean community. Researchers opted to use official data from a national survey done in the country. In their research, they do a literature review to support their claim that ADHD persists into adulthood, and given its characteristics, it ends up causing social difficulties and affective problems. It is from such realization that my urge to understand the concept emerges. I wanted to learn how such disabilities arise in adults due to the condition that has persisted throughout their growing years. This knowledge is relevant to an entire field of special education. As a practitioner, I am going to need it for effective intervention programs.


What I wanted to learn by exploring the topic/issue/disability/learning difference further

I wanted to have a deep understanding of ADHD so that I could be able to explain a number of problems with a child’s and in some cases, an adult’s intellectual, social, and psychological development (Lopez – Vergara & Colder, 2013). I was keen on finding out how behavior ends up affecting these factors in the development of a person. I wanted to see how the integration of medication and therapy in the field of healthcare and education plays a role in assisting individuals with ADHD cope with their living environment. At the same time, I wanted to learn the current situation and the emerging trends that are affecting the field of study and practice of teaching special education, with an emphasis on the effects of any present strategy on the development of a person with ADHD.

I understand that being hypersensitive is not a disorder by itself. Thus, my inquiry into this topic was mainly because this characteristic of a person occurs within another topic of attention deficit that is considered a disorder. Thus, I wanted to know how hypersensitivity and attention deficit occur and influence each other in a person’s character. Knowing this would allow me to make sense of the developments in education concerning special education, which is going to be part of my career.

Hypersensitivity is a wide topic with a variety of applicable knowledge. In this regard, it can be too confusing to work with the entire scope of hypersensitivity. Therefore, having sufficient knowledge of the topic and any related concept would allow me to narrow down to a niche of the subject, which can then serve as my basis for specializing when I am in my professional practice. It will also be a good thing to do for my additional learning needs.

After learning about hypersensitivity as a characteristic of attention deficit disorder, I wanted also to understand other characteristics of the condition. This would provide me with an all-round capacity to handle personal and organizational queries on the matter. It would also enable me to provide a convincing rationale for my career goals. Knowledge of these concepts and their prevalence in society will make me a better practitioner, and that is why I opted to explore this hypersensitivity topic further.

Further exploration urges also emerged after finding out the basic characteristics of hyperactivity like fidgeting, talking nonstop, being constantly in motion, and having difficulty in doing quite tasks and activities (Lopez – Vergara & Colder, 2013). These are also characteristics of other medical and non-medical conditions. Therefore, it is helpful to know how to identify and differentiate them to avoid misinterpretations. Correct recognition will make intervention easier. In this case, I was considering intervention in education and health care. Besides that, I have been interacting with a number of research reports and general scholarly texts on the matter.

For example, research by Park et al. (2011), sought to find out the prevalence, correlates, and comorbidities of ADHD symptoms in a Korean community. Researchers opted to use official data from a national survey done in the country. In their research, they do a literature review to support their claim that ADHD persists into adulthood, and given its characteristics, it ends up causing social difficulties and affective problems. It is from such realization that my urge to understand the concept emerges. I wanted to learn how such disabilities arise in adults due to the condition that has persisted throughout their growing years. This knowledge is relevant to an entire field of special education. As a practitioner, I am going to need it for effective intervention programs.


Roughly one-fifth of all adults with ADHD have tried cognitive behavioral therapy (CBT) and/or ADHD coaching — two popular natural treatments receiving ratings of ‘extremely effective’ or ‘very effective’ by 41% and 48% of ADDitude readers, respectively. 1 Still, some confusion persists.

CBT is a short-term, goal-oriented form of psychotherapy that aims to change negative patterns of thinking and change the way patients feels about themselves, their abilities, and their future. CBT is supported by clinical evidence and research results showing that the therapy delivers real-world benefits for adults with ADHD — namely higher self-esteem, productivity, and happiness.

ADHD coaching is an ongoing collaborative partnership created to facilitate greater self-awareness, self-regulation, and self-initiative for clients with ADHD. It is built upon unconditional acceptance and a powerful appreciation of the client’s potential, uniqueness, strengths, capabilities, and wholeness. ADHD coaches are well-versed in ADHD-specific coaching competencies. The coaching process empowers clients to accomplish personal and professional goals with customized strategies built specifically for ADHD minds.

In the recent ADHD Experts webinar “How CBT and ADHD Coaching Help Adults Manage Their Symptoms Naturally,” Dr. Russell Ramsay and David Giwerc highlighted the differences between CBT and ADHD coaching, and explained how each ADHD therapy helps mitigate symptoms of ADHD. Below, they answer some of the most common questions from ADDitude readers.

1.Where can I find accredited practitioners of both CBT and ADHD coaching?

ADHD Coaching

The following are recommended resources for finding experienced CBT practitioners:

2. Aside from checking accreditation, what should patients with ADHD look for and ask when assessing whether an ADHD coach or CBT practitioner is a good fit for them?

ADHD Coaching

The relationship between coach and client is a partnership a good fit is vital. This article presents a list of questions to ask a prospective ADHD coach. In the responses, listen for less tangible, but equally important characteristics such as style, energy, and tone from each prospective coach. This guide from the ADDCA Blog can help provide additional guidance.

I’d recommend asking about their experience working with adults with ADHD, including diagnostic evaluations and follow-up therapy. Ask about the CBT manuals or other books with which they are familiar, and their view on the executive function model of ADHD. This will also be a way to get a sense of “fit,” though that can be a different matter.

3. ADHD coaching services are often available via Zoom or other video platforms. Is the same true for CBT? Do practitioners typically accept and begin treating new patients digitally?

It depends on the state, but most are allowing cross-state services by licensed psychologists, or have made it easy to obtain a temporary license. This will likely persist after restrictions due to COVID, at least within states. There is a consortium of states through PsyPACT that will credential therapists to provide remote services across state lines for those participating states.

4. How young can an individual begin and benefit from ADHD coaching and/or CBT? Are these treatments appropriate for teens? Is it possible to be too old to benefit from ADHD coaching and/or CBT?

ADHD Coaching

Coaching is appropriate for children, adolescents, young adults, and adults. Chorological age is not a criterion for coaching it is the age level of the individual’s neurological functioning that is important. An 18-year-old may have the executive functions of a 13-year-old. A well-trained ADHD coach will support a client based on the age level of executive functioning exhibited during coaching.

Teen coaching, for example, requires customized education that is incorporated into the session in an engaging way. A teen may need to focus on a specific task, sustain their focus, and associate it with something that helps them understand it. For the teen to make progress, parents need to be educated about their child’s type of ADHD and their child’s weaknesses and strengths.

ADD Coach Academy has an accredited family training program dedicated to teaching ADHD coaches the dynamics of the family and how to best work with children of different ages who have ADHD. Coaches are only eligible for family training after they have completed the key requirements for ADHD basic coach training or ADHD advanced coach training.

ADHD coaching can also be very effective for older individuals, who are wiser in terms of experience and context. One difference may be that an older person with ADHD may need more time to access information from their long-term and working memory. A good ADHD coach would bear this in mind and provide more space and time for the older client to process and articulate their responses when questioned.

Though CBT is largely used with adults, there are some initial studies of the adult ADHD CBT approaches being “down-fitted” for older teens with ADHD. There are some CBT approaches specific to school and driving designed specifically for teens. High school-age teens with ADHD could benefit from CBT, though their receptiveness will likely be an issue.

One does not age out of CBT for adult ADHD. In fact, seniors with ADHD are a growing group, though no specialized protocols exists yet. Kathleen Nadeau, Ph.D., is currently working on a book on seniors with ADHD – her content on ADDitude might provide additional information.

5. What would you recommend for children with ADHD who struggle with executive functions, negative thinking patterns, etc.?

ADD Coaching

Working with children and their families may be the biggest segment of ADHD coaching with the largest demand. In fact, ADDCA created a specialty family training program that focuses on the dynamics of the family.

So long as children are able to communicate and be engaged in a structured but flexible coaching conversation, coaches with family training work with young children adolescents, teens college aged and young adults.

For elementary school children, parent and teacher training are still the preferred approaches. There are some CBT approaches modified for children to help with thought patterns and behaviors — for example, the past work of Phil Kendall. Richard Gallagher, Howard Abikoff, and colleagues also have a wonderful program for building organizational skills in children. The Smart But Scattered (#CommissionsEarned) series also offers a wonderful approach for executive functions, not limited to ADHD.

6. Does ADHD coaching exist for parents to teach them ways to better communicate with and guide their young children with ADHD? (Or is behavioral parent training the more appropriate choice here?)

An ADHD coach will work with parents to identify ways to communicate with their children that encourages growth, curiosity, and confidence. ADHD coaches help parents become aware of what will positively activate their child’s brain and reinforce what they can do using their strengths. The parents also must be aware of the natural sources of motivation for their child.

7. Is it necessary to have a formal ADHD diagnosis before pursuing coaching and/or CBT?

ADHD Coaching

Yes, a formal assessment or evaluation with a health care practitioner who specializes in the diagnosis and treatment of ADHD and co-occurring conditions is a vital component of effective comprehensive treatment of ADHD.

ADHD coaching is an integral component of comprehensive treatment. However, ADHD coaches are not diagnosticians. Coaching can bridge the gap between biology and behavior, but it is not the only answer. Effective treatment often includes an ADHD psychiatrist, a CBT therapist who is experienced with ADHD, and a well-trained ADHD coach.

When a coaching client is frustrated by their ability to function in specific situations, tasks, and environments, then I refer them to an MD specializing in the diagnosis and treatment of ADHD or a therapist who is experienced with the diagnostic process for ADHD and co-occurring conditions. The doctor can help the patient receive a proper diagnosis, which unlocks targeted medication at a correct dosage. Research tells us that, in 80 percent of cases of ADHD, treatment with stimulants will mitigate the impairing symptoms of ADHD. Even then, the pill does not give you the skill. But it may put a client on a level playing field to pay attention and sustain focus so they can work with a coach.

CBT focuses on problems and solutions, so even if someone does not meet diagnostic criteria for ADHD but struggles with executive functions (EF), they could likely benefit from the CBT approach for ADHD. That said, some sort of initial interview is good practice in order to determine what is causing the EF difficulties, such as an adjustment to school/work, or mood or anxiety issues, as some modification of treatment might be indicated.

8. With a diagnosis, do some insurance plans cover the cost of CBT and/or coaching for ADHD symptoms?

Most insurance plans do not cover ADHD coaching. Clients pay out of pocket. In rare cases where they do pay, Insurance companies will limit the number of sessions. This does not allow for adequate sessions to support clients. Plus, it disrupts the client’s momentum especially when they are experiencing success. ADHD coaching requires more time than life coaching to get through the invisible barriers impeding the client’s ability to create progress in different areas of their life.

9. Can you offer some guidance re: reasonable costs for CBT and ADHD coaching services? (Cost appears to be a formidable and common barrier to treatment for many people in attendance today.)

ADHD Coaching

As a general guide, ADHD coaching costs about the same as therapy or life coaching. One-hour sessions may range in price from $75 to $250, and sometimes more. There are many variables that impact the costs of coaching. The question that needs to be asked is this: How much is coaching improving the quality of my life or my child’s worth? If coaching can dramatically improve satisfaction, fulfillment, contribution, and productivity in the world, what would I be willing to pay? Costs must be addressed with each coach being considered because the cost of ADHD coaching varies.

  • There are ways to reduce the costs for ADHD coaching services. A growing number of coaches are offering a sliding-scale fee based on your level of financial comfort or a percentage of your annual income. When interviewing, ask the coach about possible alternatives to their full fee. Sometimes, if the coach and potential client have a strong connection, they might be willing to work with you.
  • If you are seeking coaching in the workplace to improve your performance or prepare for a new role, you can approach your Human Resources department and request reimbursement for the full fee or a portion of the fee. However, by doing this you are informing your company about your ADHD diagnosis. Many adults choose not to do this due to negative perceptions associated with the disorder.

Pricing for CBT depends on where one lives, private practice vs. clinic-based therapists, etc. The Penn Psychiatry Adult ADHD Program has reduced fees for trainee clinicians. Clinical psychology graduate programs often offer reduced fees for supervised graduate therapists, though it depends on the program for CBT and/or ADHD services.

10. What are some reasonable metrics for success? How can we tell if the coaching or CBT is working the way it should?

ADHD Coaching

The ADD Coach Academy participated in a study assessing the benefits of ADHD coaching for college students. The metrics of success we looked at were improvements on measures of self-efficacy, knowledge of personal learning style, and measures of self-control. Reduced procrastination, consistent completion of goals, and increased confidence in strengths were some of the observable outcomes.

What are your behavioral goals for CBT and are you meeting those goals for change? Follow-up scores on symptom and EF measures gathered during the initial evaluation can also be reviewed to assess change. Also, ask someone who lives with the patient if he or she notices a difference.

11. Can you explain the differences between CBT and DBT?

Both fall under the CBT umbrella. DBT emerged as the treatment of choice for Borderline Personality Disorder and focuses on emotional regulation and tolerating and managing emotional dysregulation, often accompanied by self-harming and suicidal behaviors. DBT comprises different coping modules that also address setting limits, asking for help, and modifying interpretations (thoughts) about feelings. DBT has been modified for adult ADHD by Alexandra Philipsen in Germany, developing coping modules geared for adult ADHD rather than the main focus on emotional dysregulation.

Acceptance and Commitment Therapy or ACT is another such “third wave” of behavioral therapies that emphasizes the ability to accept and tolerate emotional discomfort and negative thoughts without necessarily changing them as a precondition for engaging in (committing to) valued actions.

12. How long has CBT been used to treat ADHD? How ‘new’ is it, really?

The first outcome study (a chart review) of CBT for adult ADHD was published in 1999 by a Harvard group. Our program started in 1999, so it has been little over 20 years that it has been used in practice, but the past decade has seen a geometric progression of outcome studies in support of its use.

1 Frye, Davon Rodgers, Anni Layne. Special Report: How You Are Treating ADHD or ADD Today. ADDitude Magazine (2017). https://www.additudemag.com/adhd-treatment-options-caregivers-adults-survey-results/

SUPPORT ADDITUDE
Thank you for reading ADDitude. To support our mission of providing ADHD education and support, please consider subscribing. Your readership and support help make our content and outreach possible. Thank you.


References

Brydon, L., Walker, C., Wawrzyniak, A., Chart, H., & Steptoe, A. (2009). Dispositional optimism and stress-induced changes in immunity and negative mood. Brain, Behavior, and Immunity, 23, 810-816.

Gray, J. D., & McEwen, B. (2013). Lithium’s role in neural plasticity and its implications for mood disorders. Acta Psychiatric Scandinavica, 128, 347-361.

Osdoba, K., Mann, T., Redden, J., & Vickers, Z. (2015). Using food to reduce stress: Effects of choosing meal components and preparing a meal. Food Quality and Preference, 39, 241-250.

Saito, Y., & Tada, H. (2007). Effect of color images on stress reduction: Using images as mood stimulants. Japan Journal of Nursing Science, 4, 13-20.

Sherman, G., Lee, J., Cuddy, A., Renshon, J., Oveis, C., Gross, J., & Lerner, J. (2012). Leadership is associated with lower levels of stress. Proceedings of the National Academy of Sciences, 19(44). doi: 10.1073/pnas.1207042109.

Stough, C., Scholey, A., Lloyd, J., Spong, J., Myers, M., & Downey, l. (2011). The effect of 90 day administration of a high dose vitamin B—complex on work stress. Human psychopharmacology, 26, 470-476.


Introduction

In a recent theoretical review, Smith et al. (2018) eloquently describe a model outlining the ways in which emotional experiences unfold and reach awareness. This process begins with one’s affective response—i.e., the coordinated changes that occur in one’s body and cognitive or attentional state, in response to a particular situation. Affective responses can be triggered in a bottom–up fashion or alternatively by forming or reactivating perceptual representations of current, past, or imagined situations and appraising their novelty, relevance to one’s goals or values, and controllability. Cognitive and attentional habits can bias the formation of both perceptual and appraisal-based representations, and bottom–up and top𠄽own factors can shape higher-order representations of the affective response and its probable meaning.

Smith et al. (2018) go on to argue that the representations we form of the situation and our subsequent response to it can be “selected” for and actively maintained in working memory. Activating a perceptual representation of an affective response allows one to consciously experience the change in body-state that has occurred, whereas activating a conceptual representation of that response allows one to consciously recognize and describe the emotion that one is feeling (or the emotion of another person whose affective response has been simulated). Top𠄽own influences determine which (if any) of the representations formed reach conscious awareness.

The ability to generate and experience emotions is clearly evolutionarily advantageous, as they motivate us to respond in ways that can help us meet our needs. However, learning to regulate emotions is also important. According to Gross (1998a,b, 2015), adults use five main strategies (alone or in combination) to manage their emotions. Situation selection involves actively approaching or avoiding stimuli or situations that are expected to trigger particular affective responses. The remaining strategies involve top𠄽own control. People can physically alter the external environment in ways that make it easier for them to function well (situation modification). They can also use attentional deployment by shifting one’s external focus (using selective attention), or by shifting attention to calming internal thoughts or mental images (engaging working memory), one can reduce the likelihood that affective responses that make one uncomfortable will reach conscious awareness. An individual might also make a cognitive change for example, they might use verbal reasoning or reappraisal to change how they interpret an affective response. Finally, one can engage in response modulation (e.g., expressive suppression).

The models proposed by Gross (1998b) and Smith et al. (2018) can explain why our emotional experiences and our ability to self-regulate vary over time. Importantly, however, they may also help to explain individual differences in stable traits such as alexithymia. This trait, seen in approximately 10% of the general population (Mattila et al., 2010), is characterized by difficulties identifying feelings (DIF), difficulties describing feelings (DDF), an externally oriented thinking style (EOT), an impoverished fantasy life, and problems distinguishing between emotional arousal and somatic sensations (Nemiah et al., 1976). Smith et al. (2018) suggest that individuals scoring high (vs. low) on alexithymia may: (a) generate fewer or more poorly differentiated affective responses (b) perceive/represent their affective responses in a concrete or coarse-grained manner and/or (c) have developed a set of stable cognitive habits that make it difficult for them to exercise the top𠄽own cognitive control that is required for them to consciously experience their affective responses and the emotions that they are feeling. Problems in any or all of these areas would make it difficult for them to identify and describe their emotions, and this, in turn, could limit their ability to understand and regulate them.

In the present study, we explored the idea that alexithymia is associated with atypicalities in a range of bottom–up and top𠄽own processes that impact how affective responses are generated, experienced, and regulated. To do this, we collected data from a large sample of university students regarding how they process and respond to a range of body-based and environmental sensory cues and the extent to which they engage in processes not driven by environmental stimulation, such as visual imagery, dreaming, and some aspects of problem-solving. We then examined interrelationships between these measures using a variety of approaches. The first set of analyses were undertaken to examine general patterns seen in the sample as a whole. The second set of analyses explored the possibility that patterns of association between variables might differ across distinct subgroups of individuals.

Our study builds on past research suggesting that alexithymia is linked to atypicalities in sensory processing that could impact emotional embodiment. Much of the recent work in this area has focused on the ability to perceive internal body sensations correctly (interoceptive accuracy or IA). Based on their meta-analysis, Trevisan et al. (2019) concluded that there is a moderate, negative association between alexithymia and self-reported IA. Based on its links with performance on objective tests of IA, Murphy et al. (2018) argue that alexithymia may serve as an index of “multidimensional, multi-domain, interoceptive impairment” (p. 405).

Although interoceptive inputs undoubtedly contribute to embodied feelings, they cannot be the only factors that drive them, given that individuals experiencing pure autonomic failure still experience these states (Heims et al., 2004). On these grounds, we might expect alexithymia to be associated with atypicalities in the processing of a range of sensory cues. Research generally supports this idea, although the direction of effects is mixed, with some studies linking alexithymia to exaggerated neural, physiological, or behavioral responses to exteroceptive or body-based cues (e.g., Sivik, 1993 Nyklicek and Vingerhoets, 2000 Schafer et al., 2007 Bogdanov et al., 2013) and others linking it to reduced responsiveness (e.g., Pollatos et al., 2008 Goerlich-Dobre et al., 2014b Gaigg et al., 2018). Alexithymia is also associated with atypicalities in multisensory integration, although the direction of the effects has varied (see Miles et al., 2011 Thakkar et al., 2011 Cascio et al., 2012 Germine et al., 2013 Grynberg and Pollatos, 2015 Georgiou et al., 2016). The mixed results from studies in this area could reflect the fact that researchers have not typically considered in their study designs the possibility that there may be subtypes of individuals with alexithymia who generate, experience, and regulate their emotions in different ways. Exploring this possibility is important for advancing theory and research in alexithymia.

Several studies have used the 20-item Toronto Alexithymia Scale (TAS-20 Bagby et al., 1994) in combination with other measures to look for evidence of subtypes of alexithymia. Lane et al. (2015a) distinguished anomic and agnosic forms—the former being associated with problems naming emotions but intact theory of mind and the latter with problems forming conceptual representations of emotions and impaired theory of mind. In contrast, Kajanoja et al. (2017) identified a subtype characterized by strong DIF and symptoms of depression and anxiety and another characterized by elevated DDF and EOT scores and impaired empathy.

Other subtyping studies have used the Bermond Vorst Alexithymia Scale (BVAQ Vorst and Bermond, 2001), which samples both cognitive traits (the ability to identify, verbalize, and analyze one’s emotions) and affective traits (flattened affect and impoverished fantasy) that are associated with alexithymia. By applying factor analysis and principal component analyses to BVAQ scores, Bermond et al. (2007) identified a subtype characterized by high scores on both cognitive and affective dimensions (type I) and another characterized by high scores on the cognitive dimension but typical or unusually low scores on the affective dimension (type II). Although consensus is not universal (Bagby et al., 2009), most subtyping work using the BVAQ recognizes at least these two variants (e.g., Vorst and Bermond, 2001 Larsen et al., 2003 Berthoz and Hill, 2005 Goerlich-Dobre et al., 2014a). Some researchers describe a third subtype (type III) characterized by high scores on the affective dimension only (Bermond et al., 2006). Moormann et al. (2008) also recognized a lexithymic subtype (who score low on both dimensions), a modal subtype (who score in the average range on both dimensions), and a mixed class that does not fit into any category. They point out that because those with type III, lexithymic, and modal profiles do not have problems with emotional understanding and generally have good psychological health, it may be misleading to refer to them as alexithymia types.

Subtyping work using the BVAQ has been fruitful however, the distinctiveness between the cognitive and affective dimensions is not always clear indeed, there is overlap between these dimensions, particularly with regard to the 𠇊nalyzing” subscale, which taps into EOT (de Vroege et al., 2018). Preece et al. (2017) also described several limitations with the BVAQ’s 𠇎motionalizing” subscale (see also Watters et al., 2016). Another issue concerning BVAQ studies that have compared different subtypes with regard to their neural substrates (Goerlich-Dobre et al., 2015) and patterns of autonomic reactivity (Bermond et al., 2010) is that they have relied on median split procedures to create groups. The use of latent profile analysis (LPA) may be preferable, as it allows one to categorize participants in a heterogeneous sample into more homogenous subgroups based on their responses to continuous variables (Berlin et al., 2014).

In the present study, we took a unique approach to explore individual differences in alexithymia expression. Our approach was motivated by the idea (expressed by Smith et al., 2018) that two key factors contribute to the development of individual differences in people’s emotional awareness: (a) genetic/epigenetic factors and personality traits with an innate component and (b) learning, through which cognitive habits are established. The idea that differences in these factors might result in individual differences in alexithymia led us to explore links between alexithymia and sensory processing sensitivity (SPS). SPS is a genetically predetermined trait, and its expression varies as a function of life experiences (Aron et al., 2012). SPS is characterized (in part) by a tendency to become easily overwhelmed by environmental stimuli and multitasking demands and by increased sensitivity to subtle and aesthetic features of one’s environment (Aron et al., 2012). The former feature of SPS is positively associated with DIF/DDF, and the latter is negatively related to EOT (Liss et al., 2008 Rigby et al., 2020). Unlike many people with alexithymia, individuals scoring high on SPS have a “rich” inner life, which might suggest an enhanced ability to keep perceptual representations of past, current, or imagined situations active in working memory. To our knowledge, no one has explored how/if two additional features of SPS—the tendency to process information at a deep/complex level and to approach novel situations cautiously—may relate to alexithymia. Doing so is of interest, as all of the features of SPS could impact how affective responses are generated, experienced, and regulated. Indeed, in adults, all three aspects of SPS are positively associated with neuroticism and negative affectivity (Lionetti et al., 2019).

Whether or not they have SPS, individuals vary in the ways in which they typically process and regulate their responses to sensory information in daily life. Given this, we were also interested in exploring how one’s sensory processing style might impact the expression of alexithymia. Dunn (1997) has characterized trait sensory processing styles along two dimensions: neurological threshold and behavioral regulation. The former describes the amount of sensory information required to activate the central nervous system, and the latter specifies whether an individual typically responds to sensory information actively or passively. Hyposensitivity to certain kinds of stimulation may lead to a passive failure to respond (low registration or LR) or to attempts to actively seek out stimulation (sensation seeking or Seek), whereas hypersensitivity may cause one to become easily overwhelmed (sensory sensitivity or Sen) or to actively try to avoid or reduce exposure to stimulation (sensory avoidance or SA). An individual’s sensory processing style is reflected in the relative strength of their Seek, SA, LR, and Sen tendencies, which can be assessed via a self-report measure called the Adolescent/Adult Sensory Profile (AASP Brown and Dunn, 2002).

Relationships between alexithymic traits and AASP scores have been examined indirectly in several studies involving clinical populations. Co-occurring alexithymia has been shown to predict elevated scores on LR in adolescents with autism spectrum disorder (Milosavljevic et al., 2016). Bashapoor et al. (2015) observed that men with substance dependence showed heightened DIF and DDF, and elevated scores on LR, Seek, and SA, relative to a control group. Serafini et al. (2017) found that DIF and DDF scores were positively correlated with LR and that TAS-20 Total scores were positively associated with LR, Sen, and SA in adults diagnosed with a major mood disorder. Finally, Serafini et al. (2016) showed that AASP scores mediated the relationship between alexithymic traits and quality of life in participants with mood disorders. Although these findings suggest that alexithymia is linked to particular ways of processing and regulating one’s responses to sensory information, to our knowledge, no work has examined relationships between alexithymia and individual AASP scores (or patterns across these scores) in non-clinical samples.

In light of the discussion earlier, our first main objective was to examine interrelationships between alexithymia, SPS, and sensory processing styles in a non-clinical sample of young adults. In Part A later, we addressed three key questions: (1) “What are the relationships between alexithymia, SPS, and IA?” (2) 𠇍o any features of SPS improve prediction of alexithymia above and beyond that accounted for by IA?” and (3) 𠇍o sensory processing styles mediate the relationship between IA and specific alexithymic traits?” We expected to replicate past work demonstrating links between alexithymia and aspects of sensory processing beyond those supporting IA, but our approach allowed us to extend previous findings by considering multiple measures of sensory processing simultaneously.

Our second main objective was to test the novel prediction that subtypes of alexithymia could be distinguished based, in part, on aspects of sensory processing. Given the current interest in exploring links between alexithymia and IA (e.g., Brewer et al., 2016) and our own interest in studying aspects of one’s sensory processing style more generally, we included scores on the TAS-20 subscales, a measure of IA, and the AASP as input variables in an LPA. This analysis, described in Part B, allowed us to address two key questions: (1) �n subtypes of individuals be identified based on their alexithymic traits, IA, and sensory processing styles?” and, if so, (2) “How do the observed subclasses differ with regard to their latent profiles?” We expected to find that individuals could be distinguished by the relative strength of different alexithymic traits and by differences in IA and sensory processing styles. We also performed planned contrasts comparing the observed classes on measures of SPS. Finally, we examined how each of the classes scored on measures of depression, anxiety, and stress, as high scores on these measures might indicate problems with emotion regulation.


What is complicated grief?

As a general rule, when we face a loss we go through a series of stages that help us to overcome the grief. We go from a first phase of denial that allows us to soften the pain of the news, to experience great anger at the loss and sink into the deepest sadness to finally come to acceptance.

In complicated griefs, we don’t go through all these stages, we get stuck in one of them, so we don’t end up accepting the loss. Our inner world is not restructured to accept reality because we cannot get rid of recurring thoughts about the person who left us, which prevents us from getting back to life.


Anxiety in Children and Adolescents with Autism Spectrum Disorders

Anxiety and poor stress management are common concerns in clinical samples of children with autism spectrum disorders (ASD). Anxiety may worsen during adolescence, as young people face an increasingly complex social milieu and often become more aware of their differences and interpersonal difficulties. This review summarizes the state of research on the prevalence, phenomenology, and treatment of anxiety in youth with autism and related conditions such as Asperger’s disorder. Using search words autism, asperger(s), or pervasive developmental disorder and anxiety or anxious to find reports published between 1990 and 2008, this review identified 40 papers. The results of the review suggest that anxiety, whether measured categorically or dimensionally, is indeed common in children and adolescents with autism spectrum disorders and may be a source of additional morbidity. The assessment of anxiety disorders in ASD should be conducted using multiple informants and modalities, as children with ASD often do not display age-typical symptoms of anxiety. To date, relatively few controlled intervention studies using well-characterized samples have been conducted despite preliminary evidence for efficacy of select pharmacological and psychosocial approaches. Recommendations for future applied research are presented and clinical implications are explored.

Autism spectrum disorders (ASD) are characterized by deficits in social interaction and communication, as well as the presence of stereotyped behavior and restricted interests (American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders 4 th Ed. -Text Revision, 2000). Once regarded as rare, this group of disorders - which includes Autistic Disorder, Asperger’s Disorder, and Pervasive Developmental Disorder-Not Otherwise Specified (PDD-NOS), has received a great deal of professional and scientific attention. Based on recent survey findings, the United States Centers for Disease Control (2007) reported that ASD may be as common as 1 in every 152 children suggesting that these disorders pose 𠇊n urgent public health issue.”

The reasons for the increase in the estimated prevalence over the past decades are not entirely clear, but several possibilities can be advanced to at least partially explain these increased rates. First, the early studies on prevalence relied on clinically identified cases rather than community-based surveys. Cases not in treatment were therefore missed moreover, only the most severe cases were likely recorded. Second, even those studies that conducted community surveys used narrow case definitions. By contrast, more recent studies have used broader diagnostic criteria and better sampling methods, thus identifying more cases. Finally, recent studies have used better diagnostic instruments, which has served to improve differential diagnosis among the different spectrum disorders as well as helped to delineate ASD from other psychiatric disorders in children (Chakrabarti & Fombonne, 2005). As more children with ASD are identified, there will likely be a rise in the number of children and families seeking treatment. Regardless of the cause(s) accounting for the higher prevalence estimates, therefore, clinicians are now faced with increasing numbers of children and teenagers with ASD, and their families, who require assessment and effective treatment.

In the clinical setting, anxiety-related concerns are among the most common presenting problems for school-age children and adolescents with ASD (Ghaziuddin, 2002). Recognition of anxiety problems in this population is not new. Indeed, in his original description of children with 𠇌lassic” autism, Kanner (1943) noted that a number of them had substantial anxiety problems. However, the evaluation and treatment of anxiety in this population has only recently received the empirical attention it deserves. There is an urgent need for the development of effective approaches to assess and treat children and adolescents with ASD (Lord et al., 2005), including treatments addressing associated problems such as anxiety.

Currently, anxiety is not considered a phenomenological characteristic of ASD. Although it is often assumed that individuals with ASD prefer isolation and low social contact, many people with ASD are intensely aware of their social disconnectedness and appear to wish it could somehow be different (Attwood, 2000). It is logical to conjecture that the social disability associated with ASD could engender anxiety – especially in higher functioning youth who have an awareness of their social disability. If a child has a co-occurring anxiety disorder, it could compound the overall social impairment associated with ASD. For example, social anxiety may contribute to avoidance of social situations, awkward interactions with peers, and promote further isolation from same-age peers (Myles, Barnhill, Hagiwara, Griswold, & Simpson, 2001). Thus, anxiety may have bidirectional effects with the social disabilities of ASD. For these reasons, a developmental approach to understanding how anxiety develops, and how it may interact with the core disabilities of ASD, is important. This is also relevant clinically in as much as very high functioning adolescents with milder forms of ASD may present for clinical concerns due to anxiety, as opposed to the ASD per se.

An empirically based understanding of anxiety in children and adolescents with ASD is necessary to inform accurate assessment, case conceptualization, and treatment planning. To that end, this review summarizes research on anxiety in children and adolescents diagnosed with ASD. The specific aims are: (1) to summarize the empirical research on the prevalence, presentation, and treatment of anxiety in school-age children and adolescents with ASD (2) to offer guidance on the ‘next steps’ for clinical research in this area and (3) to provide clinical recommendations based on our understanding of anxiety in this population.


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

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.

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.”

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?

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 Wagerlab.Colorado.edu. 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 PainStory.science, 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.

Important Links:

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About Dr. Tor Wager, PhD

Tor 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.

The Healing Pain Podcast features expert interviews and serves as:

A community for both practitioners and seekers of health.
A free resource describing the least invasive, non-pharmacologic methods to heal pain.
A resource for safe alternatives to long-term opioid use and addiction.
A catalyst to broaden the conversation around pain emphasizing biopsychosocial treatments.
A platform to discuss pain treatment, research and advocacy.


AQA Psychology A Level Addiction

if it is not fully functioning, the nicotine stays around longer and there is more dopamine.

application: nicotine replacement therapy, which will have good implications for economy (NHS deal with less of the bad health effects that comes with cigarettes) and people are helped. However, the biological explanation takes the responsibility away from people

reductionist- which has lead to treatments but also ignores many other factors

individual differences- the other risk factors

ignores cognitive aspects (dysfunctional cognition)

Research support- Levin et al, Carter and Tiffany

dependent smokers reacted strongly to cues presented to them, reporting higher levels of craving.

scientific- the studies done are lab studies (skinner)

Practical applications- people avoid cues

Negative implications- Gambling places may make sure they encourage addiction

Other explanations- SLT to why people start it, cognitive aspects

To measure the participants objective skill levels, Griffiths recorded the gamblers behaviour. The experimenter stood nearby recording the amount of time spent there, and how much money was won

They said their their thoughts aloud while gambling

participants were then interviewed and said how much skill they thought that had


The Association Between Pre-operative Pain Psychology and Hypersensitivity With Poor Functional Outcome After Knee Replacement.

To explore whether there are factors that help us to understand why some patient outcomes are not successful and identify prediction factors for progression. Assess central pain sensitisation and psychology pre- and post-surgery with reliable tools that explore prediction tools for good/poor progression and improve patient selection, patient preparation and timing for surgery.

The aim of this project is to explore the effects of pre-surgical central pain sensitisation on pain and function outcomes post-TKA. Central pain sensitisation will be assessed using pressure algometry and the Pain Catastrophizing Scale will be used to explore pain psychology. Functional outcomes post-TKA will be assessed using a commonly used scale for patients' self-reported outcomes (Oxford Knee Score), visual analogue scale, a star excursion balance test and four recommended patient performance-based tests.


Condition or disease Intervention/treatment
Outcome After Total Knee Arthroplasty Procedure: total knee arthroplasty

Knee osteoarthritis (OA) is a major cause of disability around the world it is the most common chronic condition in primary care in the UK. By 2030 it is predicted to be the greatest cause of disability in the general population. An effective end-stage treatment for knee OA is knee-replacement surgery, which was first done in the 1970s and 1980s.

In England and Wales, the number of knee-replacement procedures recorded by the National Joint Registry in 2013 was 91,703, which represents an increase of 0.9 % over 2012. The data analysis by the National Joint Registry and the Office of National Statistics suggests that, by 2030, primary TKAs will increase by 117% from the 2012 level. Subsequently, TKA revision surgeries are expected to increase incrementally by 332%. There is a similar estimation of demand for revision TKA surgeries in the United States by 2030, they are expected to rise by 601% from the 2005 level. The United States estimation of primary TKA is for growth of 673% from the 2005 level, which is similar to England and Wales's upper-limit projections.

Post-TKA, 75-85% of patients report satisfaction with surgery outcomes, while the remaining 15-25% are dissatisfied . Total knee arthroplasty's success has traditionally been evaluated from the surgeon's perspective, e.g. the presence of surgical complications or implant survival. This is gradually changing to involve the patient in measuring health outcomes and decision-making processes. Patient-reported outcome measures (PROMs) have evolved to explore patient perspectives by monitoring the quality of care in health organizations and conducting clinical trial outcomes.

Worldwide National Joint Registry summarise the common indication for TKA revision are 29.8% due to aseptic loosening, 14.8% infection and 9.5% due to pain. Most prediction studies show that pain and psychology pre-operation may predict poor outcomes post-TKA. A systematic review by concludes that pain catastrophizing predicts chronic pain post-TKA. Pain catastrophizing is defined as a construct that reflects anxious preoccupation with pain, an inability to inhibit pain-related fears, amplification of the significance of pain vis-à-vis health implications, and a sense of helplessness regarding pain.

Chronic post-surgery pain is significantly associated with preoperational central sensitisation as in post-shoulder subacrominal decompression and hernia repair. Regarding post-TKA, a study by Lundblad et al. (2008) concluded that the preoperational hand electrical pain threshold significantly predicts pain outcomes one year post-TKA. The study explored the association between chronic pain post-TKA and preoperation widespread pain sensitisation using pressure algometry. Both study association without control the psychological confiding factor. The correlation with Western Ontario and McMaster Universities Osteoarthritis Index pain score (WOMAC) is questionable due to weakness of WOMAC with post TKA population such as low sensitivity of WOMAC's stiffness subscale reduces the overall standardized response mean and high ceiling effect Psychological pain thinking is assessed using the most widely used measuring scale: Pain Catastrophizing Scale (PCS). PCS assesses pain thinking in three dimensions: rumination ("I can't stop thinking about how much it hurts"), magnification ("I worry that something serious may happen") and helplessness ("It's awful and I feel that it overwhelms me").

The current study will investigate preoperational central sensitisation using pressure algometry, in addition to the Pain Catastrophizing Scale (PCS), to explore psychological factors. There may be some correlation between preoperational central sensitisation and post-TKA outcomes such as pain and functional improvements.

To the best of our knowledge, no previous study has explored central sensitisation using pressure algometry and the Pain Catastrophizing Scale and possible correlation with its effects on pain and function recovery post-TKA. Pain and function can be accurately assessed before and after TKA using visual analogue scale, Oxford Knee Score, balance and performance functional tests. No previous study has correlated preoperational central sensitisation and pain psychology post-TKA on the Oxford Knee Scale as commonly used patients' self-reported outcome measures.

Thus, the study may explore accurate and objective prediction factors of post-total-knee arthroplasty progression. Potentially, reliable outcome prediction could, however, improve patient selection for surgery, as appropriate timing for surgery depends on patient symptoms and efficient patient preparation for surgery if it is to be cost-effective. Accurate preoperative prediction is crucial to minimize the potential for unrealistic expectations.

Layout table for study information
Study Type : Observational
Estimated Enrollment : 50 participants
Observational Model: Cohort
Time Perspective: Prospective
Official Title: The Association Between Pre-operative Pain Psychology and Hypersensitivity With Poor Functional Outcome After Knee Replacement
Estimated Study Start Date : September 12, 2020
Estimated Primary Completion Date : February 1, 2022
Estimated Study Completion Date : December 1, 2022

Resource links provided by the National Library of Medicine


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