Those questions are not irrational. And they do not go away just because someone tells you not to worry. They are also not unique to fibromyalgia. Anyone with neuroplastic pain who has ever had an ambiguous result, an elevated marker, an image that was not quite clean, knows this feeling. The nervous system is wired to keep scanning for threats it has not fully resolved. An open medical question is exactly the kind of thing it will hold onto.

For many, these questions sit underneath everything, quietly keeping the nervous system on alert, making it hard to commit to treatment when part of you is still not sure what you are treating.

So we sat down with someone who could actually answer it.

Meet Dr. Martina Ziegenbein

We brought this question to Dr. Martina Ziegenbein, a board-certified rheumatologist trained in PRT. What makes her perspective uniquely useful here is that many rheumatologists do not have a nervous system lens. And many PRT clinicians do not have the diagnostic authority to say, with confidence, that there is nothing else going on.

Dr. Ziegenbein describes the diagnostic process in rheumatology as a fork in the road. On one side are conditions driven by measurable inflammation, where the immune system is attacking the body’s own tissue, where there is organ involvement, where the blood work and imaging show what is actually happening. On the other side are conditions like fibromyalgia, where the symptoms are real, often severe and disabling, but where the mechanism is not inflammatory tissue damage.

Rheumatologists are, in her words, a little like detectives. Their job when someone comes in with pain, fatigue, brain fog, and a list of symptoms that do not quite fit together is to figure out which side of that fork the patient is on. A fibromyalgia diagnosis is not what happens when they stop looking. It is what happens when they look carefully and come up empty on the tissue findings.

What the Tests Actually Mean

The ANA test is probably the most common source of lingering uncertainty for those with fibromyalgia. A positive ANA can be associated with autoimmune diseases like lupus, Sjögren’s disease, and systemic sclerosis. But a positive ANA is not a diagnosis of any of these things. Healthy people can have positive ANAs too.

When a rheumatologist sees a positive ANA, they do not stop there and call it an autoimmune disease. They look for the rest of the evidence. Is there inflammatory arthritis? A characteristic rash? Kidney involvement? Inflammation around the heart or lungs? Other specific antibodies that would actually point toward a particular diagnosis? Does the person’s history and physical examination fit a recognized autoimmune pattern?

Research confirms that in the absence of accompanying clinical features, a positive ANA has essentially no predictive value for an autoimmune diagnosis. Joint swelling, Raynaud’s phenomenon, certain rash patterns, specific organ involvement: these are what change the picture. A positive ANA alone, without those findings, does not.

The same logic applies to a mildly elevated ESR or CRP, some wear and tear on an X-ray, or findings that do not fit a clear pattern. These are data points that need to be read in context, not alarm bells that mean something serious was overlooked. When a rheumatologist who has done that full evaluation says fibromyalgia, they are saying: the pattern of your symptoms fits, and nothing we found points anywhere else.

Fibromyalgia has no confirmatory test. There is no blood result or scan that says yes, this is it. The diagnosis is built entirely on clinical pattern recognition: what the symptoms look like, how they behave over time, and what the evaluation ruled out. What you may have heard is: they don’t know what’s wrong with me. What your rheumatologist may have actually been saying is: I see the finding. I considered what it could mean. I looked for evidence that would make it something more serious. I did not find it.

The nervous system is not a passive bystander in this process. We already know it can produce real, measurable physiological changes in everyday life: your face flushes when you are embarrassed, your skin breaks out when you are under stress. The same principle extends further than most people realize. IBS, migraines, and even the swelling seen in CRPS are all examples of the nervous system driving genuine physical changes in the body. These are not imagined. They are real, and they are the body doing exactly what a chronically activated nervous system tells it to do. A finding on a test does not automatically mean something is systemically wrong. Sometimes it means the nervous system has been under sustained pressure for a long time.

PRT Research

Research on the nocebo effect has established that negative expectations genuinely amplify pain. The nervous system does not process a threat and a fear of a threat very differently. When the available information includes an unresolved question about whether something serious has been missed, the threat response tends to stay elevated.

For fibromyalgia specifically, the research is direct. A study following women with fibromyalgia over 10 to 12 weeks found that illness uncertainty in the presence of pain predicted greater coping difficulty, which in turn reduced coping efficacy. The unresolved question does not sit quietly in the background. It actively undermines the nervous system’s ability to regulate.

This is why getting a clear, accurate explanation of what the tests mean is not just reassuring. For many people, it is a clinical intervention in its own right.

Johnson LM, Zautra AJ, Davis MC. The role of illness uncertainty on coping with fibromyalgia symptoms. Health Psychology. 2006;25(6):696-703. doi:10.1037/0278-6133.25.6.696.

What This Means for PRT

Fibromyalgia is one of the most common conditions that brings people to PRT, and one of the most common reasons people struggle to engage with it fully is unresolved diagnostic fear. Not disbelief in the nervous system framework, but worry that the framework might not account for everything that is happening.

PRT works by helping the nervous system update its threat assessment. But when part of the nervous system is still scanning for a missed diagnosis, it stays in threat mode. And a nervous system in threat mode keeps producing the very symptoms that feel like evidence something is wrong.

If the nervous system drives physiological changes like swelling and elevated inflammatory markers in the first place, it can also reverse them. We see this clinically quite often. Patients who have had elevated markers for years watch them normalize. Swelling that seemed structural turns out to be reversible. The body is not broken. It was responding to a signal, and when the signal changes, the response changes with it.

This is part of why getting the diagnostic picture right matters so much. What Dr. Ziegenbein offers here is a clear account of how the diagnostic process actually works, what it evaluates, and why a fibromyalgia diagnosis arrived at through a careful rheumatological workup is a real answer.

PRT does not require declaring that nothing else could ever be wrong. It does not require ignoring new or changing symptoms. And it does not require absolute certainty. In fact, uncertainty and skepticism from a patient only show that they care about themselves and want to protect themselves. Sometimes, taking a reasonable step forward in treatment just requires greater clarity. For a lot of people with fibromyalgia, that clarity has simply never been offered in a way that reached them.

What This Means for Clinicians

Fibromyalgia patients who are carrying unresolved diagnostic questions represent a specific clinical situation: they understand the nervous system framework, they believe it makes sense, but when it comes to actually sitting with a sensation or practicing somatic tracking, something holds them back. A part of them is still waiting for a different answer.

A few things to note:

Ask about diagnostic uncertainty directly. Many patients have never put the specific question into words. They just know something feels unresolved. Asking directly, “Is there a test result or finding you are still wondering about?”, often surfaces something that has been quietly driving resistance to the work.

Validate before reframing. Telling a patient their positive ANA is not meaningful before acknowledging how much it has scared them tends to land as dismissal. The nervous system needs to feel heard before it can receive new information.

Consider whether a rheumatology consultation is clinically useful. For patients with significant unresolved diagnostic questions, having those questions answered by someone with the relevant expertise can do more to prepare them for PRT than additional treatment sessions.

Help patients sit with uncertainty. A thorough rheumatological workup cannot guarantee that nothing will ever change. What it can establish is that the current picture does not warrant a different diagnosis. Helping patients find a way to move forward from that, without needing absolute certainty, is often where the real clinical work is.

The goal is not to get patients to stop caring about the medical picture. It is to help them develop enough confidence in their evaluation that the nervous system can loosen its grip and tolerate a certain level of uncertainty.

Watch Dr. Ziegenbein’s TEDx Talk

How the Brain Has Power Over Our Pain

Before you go, this is worth 15 minutes of your time.

In her TEDx talk, Dr. Ziegenbein breaks down what chronic pain actually is: real, often invisible to tests and imaging, and generated by the brain rather than simply transmitted from injured tissue. She walks through how chronic pain involves changes in neural networks that process threat and meaning, and how what the brain believes a sensation means matters just as much, if not more, than the sensation itself.

The core of her argument is something PRT is built on: the brain can learn pain, and it can unlearn it. When the brain stops treating a sensation as a threat and starts treating it as safe, the signal changes.

If you have been told that your pain is real but nobody has been able to explain why, this talk is a good place to start.

Watch the TEDx Talk

Actions to Take After Reading This Newsletter

1. If you have a test result you have never been able to fully make sense of, consider whether you received a result or whether you received an explanation. Those are different things, and the gap between them is often where the unresolved fear lives.

2. If diagnostic uncertainty has been keeping you from fully committing to a nervous system approach, try naming it specifically. Not “I am worried something was missed” but “I am worried about what my positive ANA means.” The more specific the question, the more specifically it can be answered.

3. If you have been told your tests are normal without anyone explaining how they reached that conclusion, it is reasonable to ask: what would it look like if I had an inflammatory condition, and what did you look for that told you that is not what this is? That is not a confrontational question. It is a clinical one.

4. If you have physical findings that feel like evidence something structural is wrong, consider that the nervous system drove those findings. The same system that elevated your markers or produced swelling can bring them back down.

5. If you are a clinician, add diagnostic uncertainty to your intake. Ask not just what patients have been diagnosed with, but whether they believe the diagnosis, and if not, what specific question is still open. The answer often tells you more about their current nervous system state than anything else in the intake.

6. Share this newsletter with someone who has a fibromyalgia diagnosis they cannot quite trust, or anyone with neuroplastic pain who has been held back by an ambiguous test result.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

One of our readers, J. Thompson, wrote out exactly what that confusion feels like and gave us permission to share it here. We think a lot of you will recognize it.

In Her Own Words

“I feel PRT is telling me to use two opposing techniques. When sensations arise, should I pay attention to them, acknowledge them, ask what they are trying to tell me emotionally, get to the bottom of the emotion I’m suppressing, and then reassure my system that these sensations are not harmful, not to be feared, and that they are just learned neural pathways? Or am I meant to respond to the sensations with nonchalant neutrality and then move on with my day?”

The Answer Is Neither, and Both

The tension J. Thompson is describing is real. PRT does ask people to pay attention to their sensations. It also asks people not to catastrophize them, not to scan for meaning, not to treat every twinge as a message that needs to be decoded. From the outside, those two instructions can look like they are pulling in opposite directions.

But the distinction PRT is actually making is not about what you do with a sensation. It is about how you are with it.

There is a version of paying attention to your body that feels like a caring friend checking in. Gentle, curious, unhurried. And there is a version that feels like a worried doctor scanning for something wrong. Tense, urgent, braced for bad news.

From the outside, both look like they are paying attention. From the inside, they feel completely different. And the nervous system feels the difference too.

The same is true on the other end of the spectrum. There is a version of moving on with your day that is genuinely nonchalant, a light acknowledgment that the sensation is there and a return to what you were doing without alarm. And there is a version that is performed neutrality, going through the motions of not caring, white-knuckling your way through an experience you are trying very hard not to react to.

One is settling. The other is suppression in disguise.

What PRT is actually asking for lives somewhere in between. The quality of attention matters more than the technique.

What Somatic Tracking Actually Is

Somatic tracking is one of the core practices in PRT, and it is also one of the most commonly misunderstood. Part of that misunderstanding comes from the word tracking, which implies surveillance, monitoring, searching for something. But that is not quite what the practice is asking for.

Somatic tracking combines three elements: mindfulness, the ability to observe sensation without reacting to it; safety reappraisal, gently updating the brain’s assessment that the sensation is dangerous; and positive affect induction, bringing a quality of warmth, curiosity, or even lightness to the experience. The third element is the key one. Somatic tracking only works as long as you can maintain that positive emotional state. The moment it tips into anxiety or urgency, you are no longer doing somatic tracking in any meaningful sense, and you will not achieve a corrective experience. And continuing past that point carries real risk: the nervous system may read the experience as confirmation that the sensation is dangerous, or worse, as retraumatization. It is a signal to stop.

Somatic tracking is an invitation to be present with sensation without evaluating it. To notice that something is there, to stay with it for a moment with curiosity rather than alarm, and to let the nervous system have the experience of a sensation arising and nothing catastrophic following. Over time, that experience is what updates the brain’s threat prediction. The sensation arrives. The alarm does not. The brain notes the discrepancy. The threat response, over repeated experiences like this, begins to quiet.

What derails somatic tracking is not paying attention. It is paying the wrong kind of attention. When someone approaches a sensation with urgency, trying to figure out what it means, frantically searching for the emotion underneath it, scanning for a pattern that explains it, the nervous system reads that energy as confirmation that something is wrong. The practice that was supposed to create safety ends up generating more activation.

Somatic tracking is not an investigation. You are not trying to decode the sensation or hunt for a hidden meaning. You are simply being with it, lightly and without alarm. If an emotion arises naturally during that process, you can acknowledge it. But the goal is to meet it with kindness rather than anxious analysis.

What About the Emotional Work?

Our reader’s question also touches on something real about PRT worth addressing directly: the emotional component.

PRT does ask people to become more attuned to themselves, to notice what they are feeling, to develop a relationship with their emotional experience rather than overriding it. But emotional attunement is about developing an ongoing, gentle awareness over time. It is not about treating each sensation as a clue in a mystery that needs to be solved right now. The nervous system will surface what it is ready to surface when the conditions are safe enough for it to do so. Emotions do not need to be summoned or excavated on demand.

Somatic tracking is also building something over time beyond the pain-specific work. Each time someone practices being present with a sensation without reacting to it, they are developing interoception, the ability to notice and interpret the body’s internal signals accurately. For many people with chronic pain, that connection has become distorted by years of fear and avoidance. Somatic tracking, done with the right quality of attention, is part of how that connection gets rebuilt.

It is also worth addressing a belief that many people bring into this work, often from a Sarno foundation: that if they are still in pain, it means there is an emotion they have not yet found or released. That belief can drive exactly the kind of urgent emotional excavation that makes things worse. The truth is more nuanced. You do not need to uncover and release every emotion to get out of pain. What matters is not the completeness of emotional expression but the overall safety of the nervous system. A nervous system that feels safe enough will quiet the pain signal, even if there are emotions that have not been fully processed.

This is not to say that emotional work is unimportant. For many people, it is a significant part of what allows the nervous system to settle, and for some presentations, it is essential. But from a PRT perspective, the key to recovery is reducing fear and increasing felt safety in the present moment. Sometimes that requires deep emotional and trauma work. Sometimes it does not. What the nervous system needs varies from person to person, and treating emotional release as the universal answer can send people down a path of endless excavation that creates more anxiety than relief.

The distinction our reader put her finger on has actually been studied directly, and the findings explain exactly why two people can do the same practice and have completely different experiences.

Pain catastrophizing is the scientific term for what happens when attention to pain becomes fearful attention to pain. Researchers have spent decades studying it, and what they have found, consistently, is that it is not the amount of attention someone pays to their pain that predicts worse outcomes. It is the quality of that attention. The tendency to ruminate, to magnify, to feel helpless. Not more noticing. A different kind of noticing.

When someone is afraid of their pain, it captures and holds their attention in a unique way. Research on catastrophizing has also shown that high and low catastrophizers show the same initial engagement with a painful sensation, but high catastrophizers cannot disengage from it. They get stuck. That is the nervous system difference between somatic tracking done with curiosity and somatic tracking done with dread. One lets the sensation arrive and pass. The other holds on.

Brain imaging research makes the same point from a different angle. Catastrophizing does not amplify activity in the parts of the brain that process the raw sensory signal of pain. It amplifies activity in the parts of the brain that process the emotional and attentional meaning of pain. The sensation is the same. What changes is what the brain decides it means.

This matters because it means catastrophizing is not a fixed trait. It is a learned pattern of attention, and like all learned patterns, it can change. The nervous system that learned to hold on to a sensation with fear can learn to let it arrive and pass. That is exactly what somatic tracking, done with the right quality of attention, is training it to do.

The nervous system is not responding to the sensation. It is responding to what you are bringing to it.

Sullivan MJL, Bishop SR, Pivik J. The Pain Catastrophizing Scale: Development and Validation. Psychological Assessment. 1995;7(4):524-532.

Sullivan MJL, Thorn B, Haythornthwaite JA, et al. Theoretical perspectives on the relation between catastrophizing and pain. Clinical Journal of Pain. 2001;17(1):52-64.

Crombez G, Eccleston C, Baeyens F, et al. Attention to chronic pain is dependent upon pain-related fear. Journal of Psychosomatic Research. 1999;47(5):403-410.

Van Damme S, Crombez G, Eccleston C. Disengagement from pain: the role of catastrophic thinking about pain. Pain. 2004;107(1-2):70-76.

Seminowicz DA, Davis KD. Cortical responses to pain in healthy individuals depends on pain catastrophizing. Pain. 2006;120(3):297-306.

What This Means for PRT

The clinical implication of this distinction is significant, because it means that technique adherence is not the same as practice effectiveness. A patient can be doing somatic tracking, using the right words, following the right steps, and still be generating more threat activation rather than less, if the energy underneath the practice is fear and urgency rather than curiosity and warmth.

We often name this directly in session with patients who are working hard and not getting better. We reflect back that they are doing all the right things, but with an anxious energy underneath. We explain, kindly and compassionately, that the nervous system is responding to that anxiety, not to the practice.

The question to ask is not necessarily which technique should I use, or whether I am doing enough of it. Sometimes the answer is actually less. Less attention, fewer techniques, less rigid adherence to a homework checklist. For some patients, the tools themselves have become a source of pressure, something to perform correctly rather than something to experience. When that happens, the practice has been weaponized against the very nervous system it was meant to help.

For patients who notice they are approaching their practice with urgency, the answer is not to try harder to relax. That just adds another layer of urgency. It is to slow down, reduce the dose, and return to something simpler: what would it feel like to be a little kinder to myself right now? That question, genuinely asked, often shifts something that technique alone cannot.

What This Means for Clinicians

The confusion our reader described is one of the most common clinical presentations in PRT-informed work, and it rarely resolves on its own. Most patients will not find their way to the right quality of attention without someone naming it explicitly.

A few things worth holding in session:

Teach the distinction early. The difference between curious attention and anxious monitoring is not obvious to most patients. Name it explicitly. Give them a way to check themselves: does this feel like a caring friend or a worried doctor? That question is simple enough to remember and accurate enough to be genuinely useful.

Watch for effortful neutrality. Patients who describe feeling better but look braced, or who report doing the practices diligently but are not progressing, may be suppressing rather than settling. The goal is not a performative sense of calm. It is harnessing genuine ease, however small and brief at first.

Watch for over-efforting. Some patients approach their PRT homework the way they would approach a performance review. They are tracking, journaling, listening to meditations, doing every exercise, and getting worse. Ask how the practices feel to do, not just whether they are being done. If the answer involves words like “disciplined,” “consistent,” or “making sure I don’t miss a day,” that is a signal worth exploring.

Notice what the over-efforting tells you about the person. A patient who approaches their PRT homework like a performance review is often approaching the rest of their life the same way. Everything is high stakes. Everything requires maximum effort. The nervous system is probably revved up because of their overall approach to life. This can be an entry point to deeper meaningful work.

Normalize imperfect practice. Many patients treat an anxious somatic tracking session as evidence they are doing PRT wrong. Reframe it as information. The anxiety that arose is useful data about the state of the nervous system. It means the dose was too high, and that is adjustable.

The clinician’s energy matters too. A provider who approaches a patient’s symptoms with urgency, scanning for what is causing them, communicates something to the patient’s nervous system about how those symptoms should be treated. The quality of attention in the room is not one-directional.

This Week on the Pain Reprocessing Therapy Podcast

You Don’t Have to Learn to Live With It: Tinnitus, Sound Sensitivity, and the Neuroplastic Connection

The same principle this newsletter is built on, that it is not the sensation but your relationship with it that drives suffering, applies to sound too.

Host Daniel Lyman sits down with Dr. Marsha Dewey, an audiologist who founded the Tinnitus and Hyperacusis Program at Froedtert and the Medical College of Wisconsin, to talk about tinnitus, hyperacusis, and misophonia through a neuroplastic lens.

Eighty percent of people who experience tinnitus are not bothered by it. The difference between that group and the group that suffers is not the sound itself. It is the relationship with the sound. And that relationship can change.

If you or someone you love has been told to just learn to live with ringing, sensitivity, or sound reactions, this conversation is worth your time.

Listen to the Episode

Actions to Take After Reading This Newsletter

1. The next time you notice a sensation, pause before you decide what to do with it. Ask yourself honestly: what is the quality of attention I am about to bring to this? Is it warm and curious, or intense and urgent? You do not have to change what you do. Just notice the energy you are bringing to it.

2. If somatic tracking has felt like hard work, that is information. The practice is not supposed to feel effortful. If it does, try reducing the dose before you try anything else. Less time, less intensity, less frequency. See if something shifts when the stakes feel lower.

3. If you have been trying to find the emotion underneath every sensation, give yourself permission to stop. Emotions surface when the nervous system feels safe enough to surface them. They do not need to be summoned on demand.

4. If you came into this work with a Sarno foundation and have been wondering why you are still in pain despite doing the emotional work, consider that emotional release may not be the missing piece. The mechanism is nervous system safety, not emotional completion. You may be closer than you think.

5. Take an honest look at your relationship to your PRT practice. Does it feel like something you are doing, or something you are performing? If words like “disciplined,” “consistent,” or “making sure I don’t miss a day” come to mind, it may be worth asking whether the practice has become another source of pressure rather than a path toward ease.

6. Ask yourself: is this how I approach other areas of my life too? If everything feels high stakes, if maximum effort is your default, your nervous system may be responding to that pattern as much as it is responding to the pain. That is not a flaw. It is useful information about where the work might go next.

7. If you are a clinician, notice this week whether you are teaching technique or teaching the quality of attention behind the technique. Both matter, but the second one is what determines whether the first one works.

8. Share this newsletter with someone who is working hard at their nervous system practice and not getting the results they expected. Sometimes the most useful thing is to hear that the effort itself might be part of what is getting in the way.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

This week, one of our readers wrote in that she has been living with chronic pain for 12 years. She knows her pain is neuroplastic. She has worked with coaches and therapists. She is not someone who needs to be introduced to the framework. She is someone who has been living inside it, doing the work, and still struggling. And she had some questions that we think a lot of people have been sitting with quietly, afraid to ask out loud.

We asked if we could share her words and try to answer them here. We are grateful she agreed.

In a Reader’s Own Words

“I appreciate the many topics you cover in these newsletters and often find them very relevant. However, one disconnect I always feel is what happens when you cannot calm your nervous system no matter what you do? As a 12-year chronic pain sufferer who is 100% sure that my pain is neuroplastic, and who has consulted many pain recovery coaches and therapists without success, my nervous system is chronically revved, and I can’t seem to undo it no matter what I do. I think others might be able to relate to that too.”

She also sent us four specific questions. We want to answer all of them.

The Questions

1. What happens when a corrective experience goes badly and reinforces the fear instead? Or when it goes well once but not the next several times?

2. What do you do when the language of PRT feels false? When saying “I am safe” feels like a lie the nervous system does not believe?

3. Despite doing all of the nervous system work, my symptoms have actually gotten worse. More of them, more severe. I feel completely out of control. What is happening, and what do you actually say to someone in that situation?

4. At what point does “healing is not linear” stop being reassurance and become something we need to look at more honestly?

When the Approach Reinforces the Fear

Question 1: What happens when a corrective experience goes badly, or works once and then stops working?

The corrective experience model works like this: approach something your nervous system treats as dangerous, discover it is survivable, and the brain will update its threat assessment. Over time, the association between that activity and danger weakens. This works, but it does not always work in a neat line, and it is worth explaining exactly why.

The brain is a prediction machine. It is constantly generating forecasts about what is coming and updating those forecasts based on what actually happens. A corrective experience works by producing a prediction error: the brain expected danger, encountered safety instead, and that mismatch prompts an update. But the size of that update depends on how strongly the original prediction was held. In a nervous system that has been predicting danger for twelve years, a single positive experience produces a small correction against a very large prior. The update is real, but it may not be large enough to make a significant shift.

When a corrective experience does not occur, what happens is closer to what PRT clinicians call retraumatization. That word sounds alarming, but what it describes is actually straightforward: the nervous system receives confirmation of danger. It predicted a threat, and the threat arrived. This does not just maintain the original association, but strengthens it.

Then there is the harder situation, when it works sometimes and not others. When experiences are inconsistent, safe one time and painful the next, the nervous system often responds by becoming more vigilant, not less. Intermittent and unpredictable outcomes are, from an evolutionary standpoint, the most important signal to track carefully. Inconsistency tells the nervous system to stay alert. It is also worth naming that this same pattern, unpredictable reward mixed with pain, is what drives addictive behavior. The nervous system becomes almost compelled to keep trying, searching for the next moment of relief. If you have found yourself caught in a cycle of attempting the same approaches over and over despite inconsistent results, that is a predictable neurological response to an unpredictable pattern.

What this means is that the approach may need to shift before the exposure work can be productive. A nervous system that is too activated to reliably register safety during an exposure is not ready for it, regardless of how well the patient understands the rationale. In those cases, the work is not to push through. It is to bring the baseline level of activation down enough that the nervous system has the capacity to actually take in a positive signal when one arrives. Inconsistency is not evidence that healing is impossible. It is clinical information about what the system currently needs.

When the Framework Stops Fitting

The next three questions are describing the same moment: when the tools you have been given stop matching the reality you are living in.

Question 2: What do you do when the language of PRT feels false?

Let’s start with the language. “I am safe” is one of the most commonly offered phrases in nervous system work, and for many, it is genuinely useful. But telling yourself you are safe when your body is signaling otherwise can actually make things worse. The nervous system registers the mismatch between what you are saying and what you are feeling, and that incongruence can itself read as threat.

The problem isn’t language itself. PRT has always been about finding words that are accurate and authentic, language that honestly describes what is actually happening rather than trying to override it. “I am safe” becomes a problem when it functions as an attempt to talk the body out of what it is experiencing. For a nervous system in chronic activation, that statement may simply not be true yet, and the body knows the difference. The goal is to find language that is genuinely true, even if that truth is smaller to start with. “This sensation is uncomfortable, but it is not going to hurt me.” “I have felt this before and it passed.” “Right now, at this moment, nothing is actually wrong.” Those are different statements than “I am safe,” and for some nervous systems, they are the ones that can actually land.

Safety in the nervous system is not primarily a cognitive experience. It is a body experience, a bottom-up signal that arrives before conscious thought does. You cannot think your way to feeling safe if your nervous system is telling your body something different. For someone who has been trying to believe they are safe for years and cannot get there, the response is not to try harder at the same statement. It is to recognize that the entry point needs to change. There are ways into this work that do not require saying things that feel like lies: working with breath and sensation at a pace that feels survivable rather than safe, building felt safety through connection with another person rather than through self-talk, approaching the body’s signals with curiosity rather than trying to reframe them.

Question 3: What happens when symptoms get worse despite doing the work?

Now the harder questions. When symptoms are increasing in number or severity despite sustained engagement with the work, that is not a cue to keep going. It is a cue to stop and ask what is actually happening.

Early in treatment, increased symptom awareness is common and often expected. As someone begins paying close attention to body sensations, the attention itself can amplify signals. This is a phase, and it tends to be brief. New symptoms appearing in new locations can be a sign of the symptom imperative. When the nervous system’s original alarm loses its power, it sometimes shifts its attention to a new location, looking for a different way to get your attention. In that sense, new symptoms can actually signal that the original work had some effect. And the approach is the same. Just meet the new symptom the way you met the last one.

But the symptom imperative and a sign of broader underlying activation can both be true. New symptoms can indicate both: the nervous system moving to a new location, and doing so because the chronic activation driving everything was never fully reached by the treatment. When that is the case, the new symptom is not the primary problem. The underlying activation is. And that needs to become the focus before symptom-level work can take hold.

When the nervous system stays chronically activated despite sustained work, it is worth understanding what is actually driving that state. Researchers use the term allostatic load to describe the cumulative wear on the nervous system from sustained pressure over time. Under ordinary stress, the nervous system activates, responds, and returns to baseline. Under years of sustained pressure, the baseline itself shifts upward. The system reorganizes around a higher level of activation, and this is no longer simply a pain-fear cycle problem. It is a regulatory problem, and it requires a different kind of approach.

Several things can contribute to that elevated baseline. Early adversity is one of the most significant. Research on adverse childhood experiences has established that early stress or emotional unavailability alters the development of the nervous system in lasting ways. A system calibrated early for an unpredictable or unsafe environment does not simply update when the adult mind understands things differently. Much of what keeps a nervous system chronically activated is not stored as memories or beliefs that language can reach. It lives in patterns of tension, breath, and bracing that have become so familiar they go unnoticed. And then there is the cumulative weight of chronic illness itself: the appointments, the identity loss, the grief, the financial strain, the relentless effort of trying to get better. None of these are separate from the pain. They are all inputs into the same system.

For someone whose nervous system is carrying this kind of load, the path forward is not more symptom-level work. It is addressing what is driving the activation in the first place. That may mean integrating approaches that work directly with the body’s patterns of tension and activation without going through language first, like EMDR or somatic experiencing, alongside PRT work. It may mean trauma-focused work that reaches what pain-specific approaches cannot. It may mean slowing down entirely and building the capacity for regulation before attempting anything more targeted.

For some, the work also needs to include what is being held underneath the pain. The nervous system can learn that certain emotions or their expression are dangerous, and when that is the case, the pain can be partly a signal that something is being suppressed. Approaches like EAET work directly with what is being held back alongside PRT, helping the nervous system learn that feeling and expressing what is underneath is survivable. In that sense, the corrective experience is not only approaching a painful sensation. It is learning that it is safe to feel.

At WellBody Psychotherapy, many of our clinicians are trained across multiple modalities precisely because we know that for some presentations, PRT alone is not enough. If this is where you are, that is worth a conversation.

Question 4: When does “healing is not linear” stop being reassurance?

Which brings us to the question underneath all the others. At what point does “healing is not linear” stop being true and start being something we say because we do not have a better answer?

We want to be direct. There is a meaningful difference between a nervous system that is taking longer and a nervous system that needs something added to the approach. And that difference matters for how you proceed. A nervous system that is taking longer shows movement, even if it is slow and inconsistent. There may be windows of relief or moments that feel different. The overall arc, even if jagged, points somewhere.

When that movement is absent, when there has been sustained engagement with PRT-informed work over a significant period with no meaningful shift, that is not a reason to abandon the framework. It is a reason to look at what else the nervous system is carrying that the framework has not yet reached. Think of it this way: PRT works on the surface of the water. But if there is too much pressure building from underneath, from unresolved trauma, chronic stress, early adversity, the water keeps rising no matter how well you manage what is visible. The answer is not to stop working with the surface. It is to address what is building behind the dam at the same time.

For those of you in that position, you have not failed the model. The model has not yet accounted for everything your nervous system is carrying. That is a different problem, and it calls for a different conversation than to keep going. Our reader’s questions are not the questions of someone who has given up. They are the questions of someone who has stayed in the work long enough to hit its edges. Those edges are real, and they deserve real answers.

What This Means for Clinicians

The questions our reader raised are not edge cases. They are the clinical reality for a meaningful portion of the patients sitting across from you. And they deserve more than encouragement to keep trying the same approach.

A few things worth holding when working with this population:

Ask what the patient has already tried, and for how long. Someone who has been doing PRT-informed work for years without meaningful movement needs a different clinical conversation than someone who is three months in. Duration of effort matters, and it should inform how you approach the next step.

Look beyond the pain-fear cycle. For patients with high allostatic load, early adversity, or unprocessed trauma, the drivers of activation often extend well beyond the specific pain-fear loop PRT addresses directly. Assessing these factors early can help you sequence the work more effectively and avoid pushing approaches the nervous system is not yet ready to receive.

Know when to integrate other modalities. EMDR, somatic experiencing, and EAET are not alternatives to PRT. For many complex presentations, they are what makes PRT possible. Expanding your toolkit is not an abandonment of the framework. It is a deepening of it.

Be honest about progress. If a patient has been working hard without meaningful movement, they deserve to hear that directly, and to hear that this reflects the complexity of what their nervous system is carrying, not a failure of their effort or understanding.

Actions to Take After Reading This Newsletter

1. If you have been doing PRT-informed work for a significant period without meaningful movement, consider whether the approach needs to expand rather than intensify. More of the same is not always the answer. Sometimes the signal is that something else needs to come first.

2. If the language of PRT has felt false to you, try scaling it down rather than pushing through. “Right now, in this moment, nothing is actually wrong” is a different statement than “I am safe,” and for some nervous systems it is the one that can actually land. Start with what is genuinely true, even if it is smaller than you hoped.

3. If new symptoms have appeared in new locations, consider both possibilities this newsletter described. It may be the symptom imperative, a sign the original work had some effect. It may also be a signal that the underlying activation has not yet been fully addressed. Either way, it is information worth bringing to a clinician rather than trying to navigate alone.

4. If you have been working primarily at the level of thoughts and sensations, consider whether something is being held underneath that has not yet had room to be expressed. Sometimes the pain is not only a signal about danger. It is a signal that something needs to come out.

5. If you are a clinician, think about the patients in your practice who are not progressing. Ask yourself honestly whether the approach needs to expand, whether there are underlying drivers of activation you have not yet assessed, and whether integrating another modality might reach what PRT alone has not.

6. Share this newsletter with someone who has been doing the work and still struggling. Sometimes the most useful thing is to hear that their experience has a name, that there are reasons for it, and that the answer is not to try harder at something that is not working.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

It’s tempting to read that as proof something didn’t work. That you’re broken, or fragile, or that the pain was never really about the nervous system after all. For many people, that moment carries a particular kind of devastation, the quiet collapse of “I knew it was too good to be true,” the exhausting return of a story you thought you had finally left behind.

That’s not what’s happening. Something else is, and it’s worth naming clearly.

A return of pain after a period of feeling well is not a verdict. It is not proof that healing was an illusion, or that you are too damaged to stay better, or that the nervous system framework was wrong about you all along. It is the nervous system doing what it always does: responding to conditions. And when you understand what conditions it is responding to, the return of pain stops feeling like a betrayal and starts feeling like something far more useful, information that can guide you back to exactly the behaviors and patterns that got you out of pain in the first place.

The Pattern Underneath the Pain

Getting better is not an accident. The pain resolved because something changed: the way you related to your body, the way you interpreted sensation, the way you started noticing and responding to your own needs. The nervous system got the message that it was safe, and it stood down.

But old patterns have a way of coming back. Once the pain fades and life gets full again, it’s easy to forget what actually caused it in the first place. Not the injury, not the flare, but the pattern underneath it: the pushing too hard, the ignoring your own limits, the putting everyone and everything ahead of your own needs.

Those patterns changed during recovery because you were paying attention. You were doing the work, checking in with yourself, noticing the signals earlier. But once the pain resolved and life filled back up, that attentiveness can quietly fade. Not because you stopped caring, but because feeling better makes it easy to stop listening as closely. Old habits return gradually, almost invisibly, and the nervous system responds to those returning conditions the same way it did before.

This is the part worth sitting with. The pain coming back doesn’t mean healing didn’t work, or that you’re somehow fragile and prone to relapse. It usually means old patterns quietly crept back in: overriding tiredness, saying yes when you meant no, going right back to full speed without checking in with yourself. The nervous system responds to that the same way it did the first time. It’s not punishing you. It’s doing exactly what it’s built to do when those conditions return.

That reframe matters. The goal was never to become a person who never feels pain again no matter what. It’s to become someone who notices the old patterns early, before they build back up to the point where the body has to shout to get your attention again.

In July 2025, Dr. Yoni Ashar and colleagues published five-year follow-up data from the Boulder Back Pain Study in JAMA Psychiatry. The original trial had shown that 66% of PRT participants were pain-free or nearly pain-free after just four weeks of treatment. Five years later, more than half of those participants were still nearly or completely pain-free, continuing to outperform both the placebo and usual care groups.

That is a remarkable finding. It means that for the majority of people who got better with PRT, the changes held. The nervous system’s updated relationship with pain did not simply fade when the sessions ended.

But the data also contains a quieter story. Roughly 45% of the PRT group did not maintain that level of recovery at five years. The study was not designed to examine why, and the researchers do not speculate. But the question is worth sitting with, because what this newsletter is describing, the gradual return of old patterns, the fading of attentiveness, the slide back into self-neglect once life fills back up, is the most clinically plausible explanation for why some people stay better and others don’t.

Recovery from chronic pain is not a switch that gets flipped. It is a relationship the nervous system develops with safety, with the body, with the patterns of daily life. That relationship, like any relationship, requires ongoing attention. The five-year data doesn’t tell us what separates the people who stayed better from those who didn’t. But it points directly at the question, and the answer is worth looking for before the pain comes back to ask it for you.

Ashar YK, Low EL, Knight K, et al. Pain reprocessing therapy vs placebo and usual care for patients with chronic back pain: 5-year follow-up of a randomized clinical trial. JAMA Psychiatry. 2025;82(10):1049–1051.

What This Means for PRT

PRT does not end when the sessions do. That is perhaps the most important thing to understand about long-term recovery, and the thing that is most often left unsaid.

The sessions give the nervous system a new experience: that pain signals are not dangerous, that sensations can be approached with curiosity rather than alarm, that the body is safe. But what maintains that update over time is not the memory of the sessions. It is the continued practice of the behaviors and patterns that made safety possible in the first place. Noticing when you are overriding your own needs. Pausing before saying yes out of obligation. Checking in with your body before pushing through. These are not just coping strategies. They are the ongoing conditions that tell the nervous system it is still safe.

When those conditions fade, the nervous system does not hold onto the update indefinitely. It responds to what is happening now. And if what is happening now looks like the patterns that preceded the pain, the threat response has reason to return.

This is not a failure of PRT. It is how the nervous system works. It is also, importantly, good news. Because it means that a return of pain after a period of feeling well is not a sign that recovery was an illusion or that the work has to start over from scratch. It is a sign that the conditions have shifted, and that the conditions can be shifted back. The tools that worked before still work. The nervous system that learned safety once can learn it again, often faster the second time, because the pathway is already there.

The goal of PRT, understood fully, is not just to get out of pain. It is to become someone who understands what their nervous system needs and can return to those conditions when life pulls them away. That is a different and more durable kind of recovery than most people are offered, and it is available even after a relapse.

So what does that actually look like in practice? It starts with getting curious rather than panicked when pain returns. Ask yourself honestly: what has changed in how I have been treating myself lately? Am I sleeping? Am I saying no when I need to? Am I checking in with my body or overriding it? Am I doing the things that helped me feel safe, or have I quietly stopped?

Those questions are not an indictment. They are a map. And in that sense, the return of pain becomes something unexpected: a tool. Even, for some people, a kind of superpower. The nervous system that once generated pain as an uncontrollable, mysterious force is now generating it as a signal you know how to read. It is pointing you back toward the behaviors, the boundaries, the self-attentiveness that got you out of pain in the first place. That is not a small thing. It means that relapse, understood this way, is not a step backward. It is the nervous system doing its job, and you know, this time, exactly what to do with the information.

What This Means for Clinicians

When a patient comes back after a period of feeling well and reports the pain has returned, it’s worth resisting the instinct to treat this as a treatment failure or a sign the work needs to start over from scratch. It’s often more accurate, and more useful, to treat it as information.

A helpful line of questioning: “What does your life look like right now compared to when you were feeling your best? What have you stopped doing that you used to do to take care of yourself?” Patients can often answer this quickly once asked directly, even if they hadn’t connected the dots on their own. Common answers include dropping the practices that helped them feel safe in their body, taking on more than they can sustainably carry, or quietly ignoring the early warning signs they used to take seriously.

This reframes relapse from a scary, destabilizing event into a recognizable, addressable pattern. The tools didn’t stop working. Life got fuller, old habits crept back in, and the body responded the way it’s designed to. That’s not a step backward, it’s useful data about where the self-neglect crept back in.

It also helps to understand the typical arc of how patients experience relapse, because the stage they are in shapes what kind of clinical support they need.

The first stage is panic. Pain is back, and the nervous system, which had finally learned to feel safe, interprets the return as confirmation that something is wrong. Catastrophic thoughts return quickly: it didn’t work, I’m broken, I’ll never actually get better. This stage requires validation above all else. The patient needs to hear, clearly and without minimizing, that this is a known pattern, not a verdict.

The second stage is forcing it. The patient remembers the tools and tries to deploy them, but with the wrong energy. They are doing somatic tracking while bracing against the pain. They are telling themselves they are safe while their nervous system is screaming otherwise. The tools are right but the emotional state underneath them is fear, and fear is exactly what the tools are trying to address. This is worth naming in session: the goal is not to perform the practices, it is to return to the internal state that made the practices possible. Curiosity, not effort. Openness, not pressure.

The third stage is recognition: oh, this is how it works. The patient begins to connect the return of pain to the return of old patterns, to see the signal for what it is, and to understand that what got them out of pain before can get them out again. This is where the real clinical work happens, and it is often faster the second time, because the nervous system has been here before and the pathway back is already laid.

Helping patients move through these three stages, rather than getting stuck in the first two, is one of the most valuable things a clinician can do when a patient comes back in pain after a period of feeling well.

When the Body Says No

By Gabor Maté

Gabor Maté spent decades as a physician watching patients whose bodies seemed to be saying what their lives would not let them say out loud. This book is his account of what he found: that chronic illness, including chronic pain, is frequently the body’s response to sustained self-neglect, emotional suppression, and the long-term cost of putting everyone else’s needs ahead of your own. It is not a book that blames patients for their illness. It is a book that takes seriously the connection between how we live and what our bodies carry. For anyone who has recovered from chronic pain and wants to understand what to keep paying attention to, it is essential reading.

Actions to Take After Reading This Newsletter

1. If pain has returned after a period of feeling good, get curious before getting discouraged. The first instinct is often panic, and panic is the nervous system misreading the signal. Take a breath before you take a verdict.

2. Ask yourself honestly what has changed in how you have been treating yourself lately. Are you sleeping? Are you saying no when you need to? Are you checking in with your body or overriding it? Look for the small signs of old patterns returning: skipping rest, ignoring your own limits, saying yes out of obligation instead of desire, going back to full speed without pausing. These are not moral failures. They are data.

3. If you have tried reaching for the tools and they don’t seem to be working, notice what energy you are bringing to them. Somatic tracking done with bracing and urgency is a different practice than somatic tracking done with curiosity and openness. The tool is the same. The internal state matters enormously.

4. Remember that a return of pain does not erase the progress you made. The nervous system that learned safety once has not forgotten. The pathway is still there. You are not starting over. You are finding your way back to something you already know.

5. If you are a clinician, build relapse conversations around pattern recognition rather than treatment failure. Ask what changed, not what went wrong. Help your patient identify which stage they are in, panic, forcing it, or recognition, and meet them there.

6. Share this newsletter with someone who felt betrayed by their body after finally starting to feel better. Sometimes the most useful thing a person can hear is that the pain coming back is not the end of the story. It might be the most important part.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

In our July 3 issue, “When the Illness Ends but the Body Doesn’t Know It,” we misstated a finding from Hickie et al. (BMJ, 2006). We wrote that post-infectious syndrome severity was predicted by “pre-existing psychological distress and the degree of illness at the acute phase.” In fact, the study found the reverse: severity of the acute illness predicted the syndrome, while psychological and demographic factors did not, at any of the 3, 6, or 12-month follow-ups.

If anything, the correct finding makes the case for a nervous system framework stronger, not weaker. It means people don’t develop prolonged post-infectious symptoms because they were anxious or psychologically vulnerable beforehand. They develop them because their body mounted a bigger, more intense threat response to a genuinely severe illness, and that response didn’t fully stand down. That’s a biological story, not a psychological weakness story, and it’s exactly the distinction PRT rests on.

Thank you to the reader who caught this and wrote in. We appreciate everyone who holds us to the research.

There is a version of anger that most people in chronic pain know well. The kind that surfaces when someone asks, for the third time, whether you have tried yoga. The kind that flares when a doctor spends eleven minutes with you after a four-month wait. The kind that sits just underneath the surface of a conversation with someone who loves you but cannot seem to understand why you are still not better.

Most people have learned, somewhere along the way, to manage that anger. To redirect it, soften it, explain it away, or simply push it down because expressing it felt like too much, or too risky, or just not worth the energy. And for a while, that can feel like the functional choice.

But what the nervous system research suggests, and what we see in clinical work again and again, is that suppressed anger is not neutral. It does not dissipate. It goes somewhere. And in the context of chronic pain, where the nervous system is already running on high alert, that somewhere tends to be the body.

What Anger Actually Is

Before we talk about what anger does to the nervous system, it helps to say something true and simple about what anger actually is: it is information.

Anger is the nervous system’s signal that something matters. A boundary has been crossed. Something unfair has happened. A need is going unmet. Something important is being ignored or dismissed. Emotions, including anger, are also designed to move us, literally. The word “emotion” shares its root with the Latin movere, to move. Emotions are meant to push us into action: to speak, to seek, to set a limit, to change something. Anger is not, at its core, a destructive force. It is a signal. The problem is not that people in chronic pain feel angry. The problem is what happens when we don’t allow ourselves to fully feel it, when the signal arrives and gets quietly redirected before it can complete what it came to do. Acting on anger doesn’t mean directing it at someone or letting it spill over. It might mean naming it, sitting with it, letting it inform a conversation, or simply allowing it to move through the body rather than being held there.

Most of us were taught, implicitly or explicitly, that anger is dangerous. That expressing it damages relationships, makes us difficult to be around, or says something unflattering about our character. So we learn to translate it into something more acceptable: we get quiet instead of upset, we pivot to explaining instead of feeling, we tell ourselves we are not angry, we are just frustrated, and then we manage the frustration too.

This translation process has a cost. Not a moral cost, not a character cost, but a physiological one. When the nervous system generates an emotion and that emotion is suppressed before it can complete its natural arc, the activation does not resolve. The signal stays live. The body stays braced.

What Suppressed Anger Does to the Nervous System

The nervous system is not a metaphor. It is a physical system, and it responds to emotional suppression the way it responds to any unresolved threat: by staying on guard.

When anger arises and is pushed down, the body still undergoes the physiological changes that anger triggers. Heart rate increases. Muscle tension rises. The stress hormone cascade activates. The threat response is already running. What suppression does is prevent the resolution of that response, the natural discharge that would allow the nervous system to settle. The activation has nowhere to go, so it persists.

For someone already living with central sensitization, where the nervous system is amplifying signals and maintaining a heightened threat response, this matters enormously. Unresolved emotional activation is additional load on a system that is already overtaxed. The nervous system does not distinguish between a threat in the world and a threat being carried silently in the body. Both keep the alarm running.

There is also a more specific mechanism worth naming. Chronic pain is often accompanied by a significant amount of unfelt, unspoken anger: anger at the body for failing, anger at providers who dismissed the experience, anger at the illness for taking things away, anger at people who do not understand. That anger is a real and reasonable response to genuinely hard circumstances. But when it is held rather than felt, it becomes part of the nervous system’s ongoing threat load. The body knows it is there, even when the conscious mind has learned to look away from it.

A study published in The Journal of Pain followed 735 adults with chronic pain across varied diagnoses at the Stanford Pain Management Centers, assessing not just whether they felt angry, but how they experienced, expressed, and regulated anger, and whether they felt their situation was unjust. Researchers identified four distinct anger profiles using a data-driven statistical approach, and then tracked how those profiles related to pain intensity, pain interference, physical function, and disability at the time of assessment and at follow-up several months later.

The findings were consistent and clinically significant. Patients with medium to high levels of both anger and perceived injustice, those who felt their condition was unfair and that something important had been irreparably taken from them, reported the most severe pain outcomes across every measure. Greater pain intensity, more widespread pain, higher disability, and lower physical function. These effects held up even after controlling for anxiety and depression, meaning anger contributed something independent to pain outcomes, not just as a byproduct of mood.

The perceived injustice piece is worth pausing on, because it is not simply about being upset. Perceived injustice in this research reflects a specific cognitive and emotional state: the belief that one’s suffering is unfair, undeserved, and irreversible. For many chronic pain patients, that is not a distortion. It is an accurate read of an experience that has genuinely taken things away. The nervous system responds to that appraisal as an ongoing threat, which keeps the pain system activated and the body braced.

As lead researcher Dr. Gadi Gilam put it: “How patients feel about their pain, particularly whether they see it as unfair, may be just as important as the biological causes.” The clinical question, the researchers concluded, is not how to eliminate anger, but how to work with it.

Granjon M, Vest N, Mackey SC, Gilam G. Distinct multidimensional anger profiles predict current and long-term chronic pain outcomes. The Journal of Pain. 2025. doi:10.1016/j.jpain.2025.105611

A Note on This Research

Studies like this one are useful. They are also worth reading carefully.

The risk with any research linking emotional states to pain outcomes is that it can be misapplied. A finding that higher anger predicts worse pain could easily be translated, in a busy clinical setting, into the assumption that the patient’s attitude is the problem. That if they could just be less angry, or more accepting, their pain would improve. This would be a misreading of the science, and it would add another layer of harm onto an experience that already involves too much dismissal.

What the research actually shows is that unresolved anger, particularly when it is paired with a felt sense of injustice, places additional load on a nervous system that is already overtaxed. That is a physiological observation, not a character judgment. And the appropriate clinical response is not to encourage patients to suppress what they feel, but to take it seriously as a signal.

Anger in chronic pain is often a rational response to a genuinely unjust situation. Being undertreated is unjust. Being dismissed is unjust. Losing years of function and being told the tests are normal is unjust. Patients who feel that way are not catastrophizing. They are accurately perceiving their circumstances.

The goal of emotion-informed work in chronic pain is not to make patients calmer or more compliant. It is to help the nervous system process what it is carrying, so that unresolved emotional load stops amplifying an already sensitized pain system. That is a different intervention entirely, and it starts with validation, not correction.

Why Some People and Not Others

This is the question that often carries the most weight, because it so easily becomes: why am I still angry when others seem to have made peace with their pain?

The honest answer is that anger in chronic pain is almost never random. Prior nervous system sensitization, whether from earlier trauma, chronic stress, or previous experiences of dismissal, shapes how much emotional load a person is already carrying when pain enters the picture. The experience of being unheard by providers, of recovering in isolation, of receiving conflicting information about what is happening in the body, all of these are nervous system experiences that compound over time.

And sometimes there is no single obvious source. The nervous system is processing far more than the conscious mind is aware of at any given moment. A person can feel, on the surface, like they have handled things reasonably well, while their nervous system is carrying a completely different story. This is not a failure of self-awareness. It is simply how the system operates.

This means that not knowing why you are angry, or feeling like the anger is disproportionate, is not the same as the anger being without cause. It means the cause may live somewhere the thinking brain cannot easily reach. The path forward does not require excavating every source. It begins, more simply, with acknowledging that the anger is there, bringing it into awareness rather than redirecting around it, and ideally into a clinical space where it can be worked with directly.

Anger as a Signal, Not a Problem

Here is the reframe that tends to land most usefully in clinical work: anger is not the problem. The suppression of anger is the problem. And those are very different things with very different implications for treatment.

If anger is the problem, the goal is to reduce it, manage it, or replace it with something more positive. Many people with chronic pain have spent years trying to do exactly that, often because the people around them, and sometimes their providers, responded to their anger with discomfort or concern rather than curiosity.

If suppression is the problem, the goal looks completely different. It is not to have less anger. It is to allow anger to be felt, recognized, and expressed rather than stored. This is not the same as acting on anger or directing it at other people. It is the difference between feeling the emotion and holding it in the body indefinitely.

There is another layer worth naming. For many people, it is not just that anger has been suppressed. It is that anger itself has become a source of fear. The nervous system, through years of learning that anger was unwelcome, unsafe, or too much, begins to treat the emotion itself as a threat. The arising of anger triggers its own anxiety response, a bracing against the feeling before it can even fully form. In this way, the suppression is not a conscious choice. It is an automatic protective response, the nervous system doing what it learned to do.

What This Means for PRT

Pain Reprocessing Therapy works by helping the nervous system update its threat assessment, and emotional suppression is itself a form of threat. When a person has learned that their anger is unwelcome, unsafe, or too much, the nervous system carries that belief as a background condition. The ongoing effort to manage, suppress, or translate the emotion is a form of bracing. And bracing keeps the alarm on.

This is where PRT has something specific to offer. The same process that teaches the brain that physical sensations are not dangerous can be applied to emotional experience. Approaching anger with curiosity rather than alarm, allowing it to be present without immediately redirecting it, and building a felt sense of safety around the emotion itself are not just therapeutic platitudes. They are the conditions the nervous system needs to update a learned association between anger and danger. When the brain accumulates enough experience of anger arising and nothing catastrophic happening, the threat prediction around the emotion begins to quiet. The anger can finally do what it was always trying to do.

When someone is able to feel anger fully, to let it move rather than brace against it, the nervous system can complete the cycle it was already trying to complete. The signal arrives, is received, and resolves. That resolution is what allows the system to settle, which is the same settling that PRT works toward through every other avenue it uses.

This is also why so many people find, at some point in PRT work, that emotions they were not expecting start to surface. Sadness they had talked themselves out of. Grief they had managed around. Anger they had rationalized or redirected for so long that it stopped feeling like anger and started feeling like numbness. This is not a side effect. It is the nervous system beginning to process what it has been carrying.

What This Means for Clinicians

Anger in the chronic pain population is clinically common and clinically underexplored. A few things worth holding in session:

Anger often does not arrive looking like anger. It comes as flatness, as chronic low-level irritability, as a tone that is just slightly more clipped than the rest of the conversation, as reported frustration that the patient seems to be minimizing even as they name it. Learning to notice the edge of anger, and to stay curious about it rather than redirect around it, is a meaningful clinical skill in this population.

How you invite anger into the room matters as much as whether you do. For patients whose nervous systems have learned that anger is dangerous, a direct naming of it can feel like an accusation rather than an opening. Tentative, curious language tends to work better than reflective statements: “I’m noticing something in what you just said, can we slow down there?” or “What’s happening for you right now as you talk about this?” creates more safety than “It sounds like you’re angry.” The goal is to open a door, not push the patient through it.

Patients may have learned that their anger was a problem before they ever got to you. Dismissive providers, unsupportive families, and cultural expectations around illness behavior all shape how much emotional expression feels available to a person with chronic pain. The clinician’s own non-reactive presence with the patient’s anger is often what makes it possible for the patient to stay with it rather than deflect.

Be curious about what the anger is pointing at. Anger is information. When a patient expresses anger, whether at their body, their providers, their situation, or their pain, the clinical question is: what does this anger know? What need is it naming? What limit is it identifying? Following that thread often opens territory that matters for treatment.

Working With a WellBody Therapist

If this newsletter resonated, if you recognized yourself in the anger that gets managed, redirected, or pushed down before it can complete what it came to do, working with a therapist who understands the nervous system connection can make a real difference.

Suppressed anger is one of the blind spots that can keep pain going long after everything else has been addressed. A WellBody therapist can help you identify what your nervous system has been carrying, build safety around emotions that have felt dangerous or too much, and work through the layers that sit underneath the pain, not to fix you, but to help your nervous system finally finish what it started.

WellBody providers specialize in Pain Reprocessing Therapy and related approaches, and work with patients navigating exactly this kind of complexity.

Button: Get Matched With a WellBody Therapist

Actions to Take After Reading This Newsletter

1. Notice whether you have been pushing your anger away rather than allowing it to be felt. Every time we redirect or suppress anger, we send the nervous system a message that the emotion itself is dangerous. Over time, that message becomes its own source of activation, keeping the threat response running not just around pain, but around the feeling of anger itself.

2. Consider what your anger might be pointing at. Not what you should do with it, not whether it is fair or proportionate, just what it is trying to say. Anger is almost always pointing at something that matters.

3. If you notice that you feel more numb than angry, it may be that the anger has been suppressed for long enough that it has gone quiet on the surface. That is worth bringing to a provider or therapist who can help you begin to access it safely.

4. Notice whether anger feels dangerous or unwelcome to you in general. Many people with chronic pain grew up in environments where certain emotions were not safe. The belief that anger is too much, or too risky, or says something bad about you, is itself a nervous system condition that can be worked with directly.

5. If you are a clinician, notice this week whether anger comes up in session and what happens to it, whether it gets followed or redirected, by the patient or by you. And when you read research linking emotional states to pain outcomes, stay curious rather than corrective. The question is never how to get a patient to feel less. It is how to help them feel emotions more safely.

6. Share this newsletter with someone who seems to have a lot of patience with their pain and not much room for anything else. Sometimes the most useful thing a person can hear is that the feelings they have been carefully setting aside are worth picking back up.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

Far fewer people have heard of its opposite. The nocebo effect describes something just as real and, in many ways, just as important: when expectation of harm actually produces harm. Tell someone a treatment might cause nausea, and a meaningful percentage of people will report nausea, even if what they took was inert. Tell someone a diagnosis is serious and their prognosis is poor, and their nervous system responds accordingly, sometimes amplifying the very symptoms that diagnosis was meant to explain.

This is not a character flaw or a sign that someone is suggestible in some weak-minded way. It is the nervous system doing exactly what it is built to do: taking in information about threat and danger and adjusting the body’s output accordingly. And once you understand that mechanism, a lot of experiences that felt confusing or hard to explain start to make a different kind of sense.

What Placebo and Nocebo Actually Are

Placebo and nocebo are often described as if they are opposites operating on separate tracks, but they are really the same mechanism pointed in different directions. Both describe the brain’s expectation shaping the body’s actual physiological response.

The placebo effect is well documented in the treatment of pain specifically. Patients given an inert treatment, but told it will reduce their pain, often show measurable reductions in pain intensity, and in some studies, measurable changes in brain activity in regions associated with pain processing. The body is not simply imagining relief. Something physiological is happening, triggered by the expectation of relief itself.

The nocebo effect works through the identical pathway, just inverted. If a person expects a treatment to cause side effects, expects a diagnosis to mean a worsening trajectory, or expects a movement to cause pain because they have been told their body is fragile or damaged, the nervous system treats that expectation as information. It primes the threat response. It can genuinely produce the symptom that was feared.

This is why language in clinical settings matters so much more than it is often given credit for. A provider who says “your spine looks like it belongs to an eighty year old” or “you may never be pain-free again” is not just delivering information. They are giving the nervous system a threat cue, and the nervous system responds to threat cues by generating more protective output, which often means more pain.

PRT Research

[PRT Research image here]

For years, clinicians have observed that fear, anxiety, and negative expectations can make a patient’s pain and treatment outcomes meaningfully worse. What has been harder to pin down is exactly how this happens inside the brain, and whether it represents a real biological process or something closer to a patient’s perception.

A new study published in Nature Communications by researchers at the University of Toronto Mississauga and McGill University has identified the specific brain pathway responsible. The two labs arrived at the same finding independently, without coordinating their research, which makes the convergence especially notable. Both identified a neurochemical called cholecystokinin, or CCK, as the key driver of nocebo pain.

The researchers traced the exact path CCK travels. It originates in the anterior cingulate cortex, the part of the brain that processes the emotional dimensions of pain, and moves down to a midbrain structure called the lateral periaqueductal gray, where it directly increases pain sensitivity. In effect, this pathway functions as a volume control. When the brain registers fear, anticipation, or a negative expectation, it turns the dial up, and pain that might otherwise register as mild becomes significantly more intense. For those of you who have been with us for a while, this one might feel particularly satisfying. We talk about the brain turning up the volume on pain, about amplification and threat signals, week after week. This study shows exactly what that looks like inside the brain: the specific pathway, the specific chemical, the specific switch.

Using behavioral, pharmacological, and optogenetic methods, the researchers were able to switch this circuit on and off directly. Activating the pathway increased pain sensitivity. Blocking it prevented the nocebo response from occurring at all. This is what makes the finding so significant. It is not an inference based on self-report. It is a demonstration that the nervous system mechanism is real, physical, and controllable.

Dr. Loren Martin, one of the study’s senior authors, was direct about what this means for patients. “Nocebo-related pain amplification is not simply imagined or exaggerated,” he said. “The brain is actively generating a real biological pain response through specific neural circuitry.” That volume knob we talk about is not just a metaphor. It is a measurable, physical circuit, and now we know exactly where it is.

Poulson SJ, Skvortsova A, Zahra FT, et al. Cholecystokinin input from the anterior cingulate cortex to the lateral periaqueductal gray mediates nocebo pain behavior in mice. Nature Communications. 2026.

Is It Still Treatment If It Works?

This is the question that comes up almost every time placebo gets discussed seriously, and it deserves a real answer rather than a dodge.

If a person’s pain improves because they believed a treatment would help them, even when the treatment itself had no direct pharmacological or structural effect, is that still treatment? Is the improvement less real?

We want to be direct about this: no. Improvement produced through the placebo pathway is not imaginary, and it is not a lesser kind of healing. It is happening through the same nervous system mechanisms that PRT is built on. The pain reduction is measurable. The functional improvement is measurable. The fact that the pathway runs through expectation and belief rather than through tissue repair does not make it fake. It means the nervous system was the lever the whole time.

Where it gets more complicated, and where we want to be careful, is in distinguishing this from the suggestion that all chronic pain is “just placebo” or “just in your head,” which is a misreading of the science and, frankly, a harmful one. The nervous system mechanisms that drive placebo and nocebo responses are the same mechanisms that drive central sensitization, that drive symptom amplification after injury, and that drive the persistence of pain long after tissue has healed. Understanding placebo does not mean dismissing pain as imaginary. It means recognizing that the nervous system has more influence over the pain experience than the purely structural model ever accounted for, and that this influence can be worked with deliberately, rather than left to chance or to the accidental nocebo effects of a rushed clinical conversation.

We are asked constantly whether chronic pain is real. Now we find ourselves asking the same question about treatment. And the answer, it turns out, is the same in both cases. The nervous system is real. The expectations it forms are real. The pain they generate is real. And the relief that comes from changing those expectations is just as real. The fact that the mechanism runs through the brain does not make it imaginary. It makes it biology.

PRT does not rely on placebo in the sense of deception or inert treatment. It works directly and transparently with the mechanism that placebo and nocebo research has revealed: that the nervous system’s expectation of safety or threat shapes the pain experience. The goal is not to trick the nervous system. It is to give it accurate information that allows it to stand down.

What This Means for PRT

Once you understand nocebo, a lot of what happens before a patient ever walks into a PRT-informed treatment room comes into focus. Many patients arrive having already absorbed years of nocebo input: scary diagnostic language, warnings about fragility, prognoses that left little room for hope. Their nervous system has been primed, again and again, to expect continued threat.

Part of the work of PRT is, in effect, reversing that priming. Helping patients understand that their pain does not indicate ongoing damage. Helping them recognize that previous warnings, however well-intentioned, were often inaccurate or incomplete. Replacing threat-based information with safety-based information is not wishful thinking. It is using the same mechanism that drove the nocebo effect, in reverse.

This is also why language inside the treatment itself matters so much. The way a provider talks about a patient’s body, their prognosis, and their capacity for change is not neutral. It is either reinforcing the nervous system’s threat response or helping to interrupt it. Every session is an opportunity to replace a nocebo with something more accurate.

What This Means for Clinicians

Nocebo effects are, in large part, an unintended byproduct of clinical communication, which means they are also within a clinician’s control to reduce.

A few things worth holding when working with this population:

Check your language for threat cues. Phrases like “degenerative,” “bone on bone,” “your disc is herniated,” and “you’ll have to learn to live with this” carry weight that often exceeds their clinical accuracy. Many of these findings are common in pain-free populations. Consider how the same information could be communicated without inadvertently installing a nocebo response.

Informed consent does not require frightening language. Patients have a right to understand risks and realistic outcomes, but there is a meaningful difference between accurate, balanced information and language that maximizes threat. The research on nocebo suggests that how risk is framed changes the actual rate of adverse outcomes, not just the patient’s perception of them. In practice, this might mean leading with what is likely rather than what is worst-case, using neutral descriptive language rather than alarming labels, and pairing any difficult information with an honest account of what is possible. The goal is not to sugarcoat. It is to inform without priming the nervous system for failure.

Ask what patients have already been told. Many patients carry nocebo-primed beliefs from previous providers, imaging reports, or even well-meaning family members. Uncovering and directly addressing those beliefs is often necessary before new, more accurate information can take hold.

This is not about toxic positivity. Acknowledging nocebo does not mean pretending all diagnoses are equally benign or that real risks should be minimized. It means recognizing that the way information is delivered is itself a clinical variable, one with measurable effects on outcomes.

Reading Corner

The Nocebo Effect: When Words Make You Sick

By Michael Bernstein, Charlotte Blease, Cosima Locher, and Walter Brown, Mayo Clinic Press

In the early 1960s, dozens of workers at a US textile factory grew dizzy, nauseated, and were hospitalized in what became known as the June Bug outbreak. Investigators found no bug, no toxin, no physical cause at all. What spread through that factory was expectation. Workers heard their colleagues were getting sick, expected to get sick themselves, and then genuinely did.

It is one of the most striking documented cases of the nocebo effect, and it is where this book begins. Written by four researchers at the forefront of placebo and nocebo science, it is the first book dedicated entirely to the subject. Accessible enough for patients, rigorous enough for clinicians, and relevant to anyone who has ever wondered how much the words we hear about our health shape the health we actually experience.

Button: Get the Book

Actions to Take After Reading This Newsletter

1. Think back to a diagnosis or piece of medical information you were given that scared you. Consider whether that fear was proportionate to the actual finding, or whether the way it was communicated made it sound worse than the underlying reality.

2. If you have been told your body is fragile, damaged, or unlikely to improve, consider seeking a second opinion or a more current understanding of what that finding actually means for your recovery.

3. Notice the language you use about your own body. If you regularly describe yourself as broken, damaged, or doomed to a certain outcome, that language is not neutral. It is information your nervous system is taking in and responding to.

4. If you are a clinician, review how you typically deliver diagnostic or prognostic information. Consider whether there are ways to communicate accurate information without maximizing threat language.

5. Notice if you have been treating placebo as a dismissive term. The research suggests it points to something real and powerful about how the nervous system works, not evidence that someone’s pain was never legitimate.

6. Share this newsletter with someone who has been carrying around scary medical language for longer than is serving them. Sometimes the most useful thing a person can hear is that the way something was said to them may have done more harm than the finding itself.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

And if you are anything like many of the people we hear from, your response to that advice was something close to: okay, but how? And also, will it actually help?

Those are the right questions. And they are especially worth asking for the particular kind of person who tends to end up in chronic pain. In our clinical experience, people with chronic pain are often high achievers, perfectionistic, and type A. They are used to pushing through, holding it together, and getting things done. For that kind of nervous system, self-compassion does not just feel unfamiliar. It can feel like a waste of time, or even a step backward.

But biology tells a different story. There are documented mechanisms that explain why the way you relate to yourself, especially in moments of pain and struggle, has a measurable effect on your nervous system, your pain experience, and your capacity to heal. This week, we want to walk you through what those mechanisms actually are.

What Self-Criticism Does to the Nervous System

Before we can talk about what self-compassion does for you, it helps to understand what its opposite is doing.

When you speak harshly to yourself, when you berate yourself for being in pain, for not recovering fast enough, for canceling plans again, for not being able to push through the way you used to, your nervous system registers that as a threat. Not metaphorically. Literally. The same neural pathways that activate when you sense danger in your environment activate when the danger is coming from your own inner voice.

This matters enormously in the context of chronic pain, because your nervous system is already in a heightened state. It is already scanning for threat, already amplifying signals, already working overtime to protect you from something it has decided is dangerous. Self-criticism does not motivate you to heal faster. It adds more fuel to a fire that is already burning too hot.

Research on the relationship between self-criticism and pain has shown that people who score higher on measures of self-judgment report greater pain intensity, higher levels of catastrophizing, and lower functioning than those who respond to their own suffering with more kindness. This is not because self-compassionate people have less severe conditions. It is because the nervous system of someone who feels safe in their own mind is operating differently than the nervous system of someone who is constantly under attack from within.

PRT Research

[PRT Research image here]

Self-compassion as a clinical construct was developed largely through the work of researcher Kristin Neff, whose model identifies three components: self-kindness rather than self-judgment, a sense of common humanity rather than isolation, and mindfulness rather than over-identification with painful thoughts or feelings.

What is particularly relevant to pain reprocessing is what self-compassion does physiologically. Studies have found that people higher in self-compassion show lower levels of interleukin-6, an inflammatory marker, in response to acute stress, suggesting that self-compassion does not just change how we feel, but how the body responds at a biological level. Separate research using compassion-focused imagery has linked the practice to increased heart rate variability, a measure of parasympathetic nervous system activity, and in some participants, reduced cortisol.

Studies using fMRI have added another layer to this picture. Self-criticism has been shown to activate the brain’s threat and punishment systems, while self-reassurance activates a distinct set of neural regions. The nervous system does not treat your inner voice as neutral background noise. It responds to it the same way it responds to any other signal from the environment.

For people in chronic pain, the implications are direct. A nervous system running on self-criticism is generating more threat and amplifying pain. A nervous system that feels safe in its own inner environment has better conditions for recovery.

Neff, K. D. (2003). Self-compassion: An alternative conceptualization of a healthy attitude toward oneself. Self and Identity, 2(2), 85–101.

Breines, J. G., et al. (2014). Self-compassion as a predictor of interleukin-6 response to acute psychosocial stress. Brain, Behavior, and Immunity, 37, 109–114.

Longe, O., et al. (2010). Having a word with yourself: Neural correlates of self-criticism and self-reassurance. NeuroImage, 49(2), 1849–1856.

Rockliff, H., et al. (2008). Heart rate variability and cortisol responses to compassion-focused imagery. Clinical Neuropsychiatry, 5(3), 132–139.

The Misconception That Keeps People Stuck

Here is where we want to push back on something, because it comes up constantly.

Many people resist self-compassion because they believe, at some level, that being hard on themselves is what keeps them functional. That if they stopped criticizing themselves for struggling, they would stop trying. That self-kindness is the same thing as giving up, lowering the bar, or refusing to take responsibility.

This is one of the most common and most costly misunderstandings we encounter.

The research is consistent on this point: self-compassion is not associated with reduced motivation, lower standards, or passivity. It is associated with greater resilience, higher willingness to try again after failure, and better long-term outcomes. People who respond to setbacks with self-compassion are more likely to persist, not less.

In the context of pain, this shows up in a specific and important way. The person who berates themselves for a flare-up is more likely to catastrophize, to fear the next flare, to have their nervous system escalate its threat response ahead of any new challenge. The person who can meet a flare with something closer to “this is hard, and I can get through it” is giving their nervous system information it desperately needs: that the present moment, even a difficult one, is survivable. That distinction is the difference between a nervous system that escalates and one that begins to recalibrate.

What Self-Compassion Actually Sounds Like

This is where it tends to get abstract, so let’s make it concrete.

Self-compassion does not sound like “everything will be okay” or “look on the bright side.” It does not require believing things are better than they actually are, nor does it require self-pity.

It sounds more like: “This is really hard right now.” “Of course I’m frustrated. Anyone would be.” “I’m doing the best I can with what I have today.” Just an honest acknowledgment that what is happening is genuinely difficult, offered with the same basic warmth you would extend to someone you care about going through the same thing.

A useful question to carry into a hard moment: would I say this to a friend? Most people who cancel plans because of pain would never say to a close friend in the same situation: “You are such a burden. Why can’t you just push through?” And yet that is often the exact tone of their own inner voice.

This short video makes that gap impossible to ignore. People are asked to share some of the harsh and unfiltered things they say to themselves. Then they are asked to say those same words to a photo of themselves as a child. Nobody can do it. The exercise lands because it makes visible something we usually keep invisible: that the voice we direct at ourselves in pain is one we would never aim at someone we loved. And the voice you would use with that child is exactly the one you deserve now rather than the one you have been using.

The practice is not complicated. It is noticing that gap and beginning, slowly, to close it.

If you want somewhere to start, Kristin Neff developed a simple practice called the Self-Compassion Break. It takes about thirty seconds and works by hitting three levers at once: acknowledge what is hard (”this is a moment of suffering”), recognize you are not alone in it (”suffering is part of being human, others feel this way too”), and offer yourself something kind (”may I give myself what I need right now”). Small, repeatable, and grounded in the same nervous system science we come back to every week.

What This Means for PRT

Pain Reprocessing Therapy works by helping the nervous system update its threat assessment. It teaches the brain that sensations that have been coded as dangerous are actually safe. And self-compassion is part of that work.

When a patient can begin to meet their own pain with curiosity rather than fear, with kindness rather than contempt or self-criticism, they are actively changing the conditions under which the nervous system is operating. Self-compassion reduces threat load and signals safety. And safety, as we return to again and again in this work, is what the nervous system needs to begin to settle.

This is why PRT does not simply teach techniques and send people home to practice them in isolation. The relationship a patient has with themselves, the tone of their own inner voice when things are hard, is itself a nervous system input. Working with that voice, not to silence it but to shift its register from threat to care, is part of what makes recovery possible.

For many patients, this is actually the hardest part of the work. Changing the relationship to pain is one thing. Changing the relationship to themselves is another. But the two are not as separate as they seem. Learning to say “of course this is hard” instead of “what is wrong with me” is not just kindness for its own sake. It is, quite literally, therapeutic.

What This Means for Clinicians

Self-compassion shows up as a meaningful variable across depression, anxiety, chronic pain, eating disorders, and trauma recovery. It is worth building into your clinical framework not as an add-on, but as a foundational condition for change.

A few things worth holding when working with this population:

The inner critic often sounds like a protector. Many patients who are highly self-critical developed that pattern as a way to stay safe, stay small, avoid disappointing others, or maintain a sense of control in unpredictable environments. Challenging self-criticism without acknowledging its original function can feel threatening. Meeting it with curiosity often works better than meeting it with correction.

Self-compassion is not the same as reassurance, and it helps to keep that distinction clear in session. Reassurance tells a patient that things will be okay. Self-compassion does something different: it helps them be with how things are right now, without judgment or self-attack. The goal is not to make the pain seem smaller. It is to help the person feel less alone with it.

Modeling matters. How you respond to a patient’s self-criticism in session shapes what feels possible to them. A clinician who mirrors back warmth and non-judgment in the face of a patient’s harshest self-assessments is teaching something that no amount of psychoeducation can fully replace.

The good news is that self-compassion is trainable. It responds to practice. Patients who feel hopeless about their capacity for self-kindness are often surprised by how much can shift with deliberate attention over time.

Ready to Work With Someone Who Gets It?

At WellBody Psychotherapy, the relational work of shifting your nervous system’s relationship to itself is at the heart of how recovery happens. If you are ready to work with a provider who understands chronic pain from the inside out, WellBody is accepting new patients.

Button: Schedule an Intake

Reading Corner

The Pain Reprocessing Therapy Workbook for Teens

By Daniella Deutsch, LCSW, and Paulina Soble, LCSW

If the young person in your life is living with chronic pain, this one was written for them. It takes the same nervous system science we cover every week and translates it into something a teenager can actually use, with step-by-step practices, worksheets, and audio tools that make the concepts concrete and accessible. Worth keeping on your radar whether you are a parent, a teacher, a coach, or a clinician working with younger patients.

Get the Workbook

Actions to Take After Reading This Newsletter

1. Notice the tone of your inner voice the next time you are in pain or struggling with a symptom. You do not have to change it right away. Just notice it. Is it speaking to you the way you would speak to someone you love who was going through the same thing?

2. If the answer is no, try one sentence. Not a mantra, not a full reframe. Just one sentence that acknowledges what is hard without adding judgment. “This is really difficult right now” is enough to start.

3. If you have been telling yourself that being hard on yourself keeps you motivated, consider whether the evidence actually supports that. Has self-criticism moved you toward healing, or has it added a layer of suffering to an experience that was already painful enough?

4. If you are a clinician, pay attention to how your patients talk about themselves in session. Self-criticism often hides in plain sight, framed as honesty or realism. Naming it gently and distinguishing it from useful self-reflection can open significant clinical ground.

5. Notice whether self-compassion feels selfish or weak to you. That feeling is worth examining. The research suggests it is one of the most effective things you can do, not just for your emotional wellbeing, but for your nervous system and your pain.

6. Try Kristin Neff’s Self-Compassion Break the next time you are in a hard moment. Acknowledge what is hard (”this is a moment of suffering”), recognize you are not alone in it (”suffering is part of being human”), and offer yourself something kind (”may I give myself what I need right now”). The whole thing takes thirty seconds.

7. Share this newsletter with someone who is hard on themselves about their pain. Sometimes the most useful thing a person can hear is that the voice telling them they should be better by now is not telling the truth.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

Perhaps the symptoms shifted or faded and then came back. Maybe the fatigue never really lifted and the pain moved around or settled somewhere it had no structural reason to be. You saw doctors and ran tests that all came back normal. And somewhere in that process, someone may have suggested that what you were experiencing was anxiety, deconditioning, or simply the new normal you would have to learn to live with.

We want to say something clearly before we say anything else: we believe you. The illness happened. The symptoms are real. The fact that the tests don't fully explain what you're experiencing does not mean there is nothing to explain. It means you may need a different framework. And this week, we want to shine a light on it.

The Acute Phase Was Exactly What It Looked Like

When the body is fighting an infection, the immune system launches a full-scale response. Inflammatory signals course through the bloodstream, the nervous system shifts into high alert, and the brain, reading all of this as danger, does what brains do under threat: turns up the volume on pain, pulls energy away from anything nonessential, and makes rest feel mandatory. The result is fatigue that pins you to the couch, aching that makes your whole body feel wrong, and a fog that makes it hard to follow a conversation. That is all because the body is doing its job, conserving resources and forcing stillness so the immune system can do its work.

For most people, that response winds down when the pathogen clears. The immune system stands down, the nervous system gradually returns to baseline, and the symptoms resolve. The body heals and you go back to life.

But sometimes that return does not happen. And the question of why is where things get interesting.

What Lingers After the Infection Is Gone

The pattern appears across a striking range of infections: Epstein-Barr virus, the virus behind mononucleosis; Borrelia burgdorferi, the bacteria transmitted by tick bites; SARS-CoV-2. Different pathogens, immune profiles, and affected populations. And yet the post-infectious picture that emerges in a subset of patients looks remarkably similar across all of them: fatigue that you can’t sleep away, diffuse pain, cognitive difficulties, and symptoms that fluctuate without clear structural explanation.

What the research increasingly suggests is that a significant driver of this persistence is not the ongoing presence of the pathogen, but what the infection taught the nervous system. During a serious illness, the nervous system learns quickly and efficiently to treat incoming signals as dangerous. Its threat-detection systems amplify. It becomes hypervigilant. And in some cases, that learned response outlasts the illness that triggered it.

This does not indicate a damaged or broken nervous system. In fact, the opposite is true. It did exactly what it was designed to do: protect the body from a threat that, at the time, was very real. The problem is that the nervous system has not yet received the update that the threat has passed and it is safe to stand down.

This learned state is known as central sensitization, in which the central nervous system remains in a heightened, reactive mode even after the original source of danger has resolved. The nervous system, trained during the infection to treat incoming signals as threatening, continues to amplify those signals. Pain that might otherwise register as mild becomes severe. Fatigue that would normally resolve with rest persists. Sensations that would typically go unnoticed feel overwhelming. The infection is gone, but the nervous system is still responding as if it isn’t.

PRT Research

In a landmark study published in the BMJ, researchers followed patients recovering from three different infections: Epstein-Barr virus, Q fever, and Ross River virus.

Despite the very different nature of these pathogens, a similar subset of patients across all three groups developed prolonged post-infectious fatigue, with symptoms including musculoskeletal pain, neurocognitive difficulties, and mood disturbance.

Interestingly, the severity of the post-infectious syndrome was not predicted by the severity of the initial illness, but rather by pre-existing psychological distress and the degree of illness at the acute phase. The pathogen appeared to be the trigger, not the ongoing cause.

The picture emerging from Long COVID research carries similar themes. A 2020 paper found that many Long COVID patients meet criteria for central sensitization syndromes, including fibromyalgia, and that the symptom profile maps closely onto what the pain field has documented in post-infectious contexts for decades. The authors were careful to note that Long COVID is likely heterogeneous, meaning different mechanisms may be at work in different patients. We want to share that same caution here. The science on Long COVID is still evolving rapidly, and we cannot say central sensitization accounts for all of it at this time. What we can say is that it accounts for some of it, and that for those patients, a nervous system lens opens treatment doors that a purely structural approach does not.

Hickie I, Davenport T, Wakefield D, et al. Post-infective and chronic fatigue syndromes precipitated by viral and non-viral pathogens. BMJ. 2006;333(7568):575.

Clauw DJ, Häuser W, Cohen SP, Fitzcharles MA. Considering the potential for an increase in chronic pain after the COVID-19 pandemic. Pain. 2020;161(8):1694-1697.

Why Some People and Not Others

This is the question that often carries the most weight for patients, because it so easily becomes: why me?

The honest answer is that we don’t fully know. But the research points toward several factors that appear to matter. Prior nervous system sensitization, whether from earlier trauma, chronic stress, or previous pain experiences, seems to raise the likelihood of post-infectious persistence. The emotional and psychological context at the time of illness matters too. People who experienced significant fear, uncertainty, or distress during the acute phase appear to be at higher risk for prolonged symptoms afterward. This is not about being weaker or more anxious than someone who recovered quickly. It is about the nervous system arriving at the infection already primed, and the infection tipping it into a state it struggles to exit on its own.

The experience of the illness itself plays a role as well, not just whether it happened, but what it was like to live through. Being dismissed by medical providers, recovering in isolation, feeling frightened without a clear explanation, receiving conflicting information about what was happening in the body. All of these are nervous system experiences layered on top of the physical one. A person whose illness was accompanied by significant confusion or a sense of being unsupported is giving their nervous system additional reasons to stay on alert, long after the pathogen has cleared.

And sometimes there is no obvious answer, even when you look for one. The conscious mind can only hold so much at once. But the nervous system is processing far more than we are ever aware of at any given moment: scanning for threat, tracking patterns, holding experiences the conscious brain may have no access to. A person can feel, on the surface, like they are handling things, while their nervous system may be carrying a completely different story. This is not a failure of self-awareness or a sign of hidden pathology. It is simply how the nervous system operates. It does not require the conscious mind to sign off before deciding to stay on guard.

This means that not knowing why your system is sensitized is not the same as there being no reason. It means the reason may live somewhere the thinking brain cannot easily reach. The path forward does not require digging for an answer. PRT does not require patients to identify the source of every alarm. It works with the nervous system directly, wherever it is, and helps it learn that the present moment is safe.

Understanding this does not mean the illness was not real, or that the prolonged symptoms are less real. It means that the “why me” question, as painful as it is, is actually pointing somewhere useful: toward history, context, and the state of the nervous system at the time. And those are exactly the things that a nervous system-informed approach like PRT can address.

What This Means for PRT

Pain Reprocessing Therapy is built on the premise that the nervous system can learn to generate pain and symptoms in the absence of ongoing tissue damage, and can therefore be taught to respond differently. Post-infectious syndromes are, for many patients, precisely this situation. The infection started something, but the nervous system is what’s keeping it going.

The work in PRT does not ask patients to dismiss what happened to them. In this case, it can start from recognizing that the illness was real and that the nervous system’s response was logical. And now we are going to help the nervous system update its threat assessment. That distinction matters enormously in this population, because so many of these patients have been told, in various ways, that what they’re experiencing is in their head. Instead of repeating that message, PRT validates the experience and then offers a path forward.

For patients with post-infectious symptoms, PRT often begins with simply naming the mechanism. Hearing that there is a documented biological explanation for why symptoms persist after an infection resolves, one that does not require an ongoing pathogen and does not imply psychological weakness, can itself begin to reduce the nervous system’s threat response. For many patients, that explanation alone is the first moment of genuine relief they have had since getting sick. Often, it is the first time anyone has offered them a framework that does not end in “we don’t know” or “learn to live with it.” When the nervous system finally feels understood rather than dismissed, something begins to shift. Safety is what turns hypervigilance down, and understanding is often where safety starts.

What This Means for Clinicians

Post-infectious syndromes are some of the most clinically challenging presentations precisely because they fall between specialties. Infectious disease has cleared the pathogen. Rheumatology has ruled out autoimmune involvement. Neurology has found nothing structural. And the patient arrives with a thick file and a look that says: no one has been able to help me.

A few things worth holding when working with this population:

Ask about the onset. When patients present with chronic fatigue, widespread pain, or medically unexplained symptoms, ask directly: Was there an illness that preceded this? Many patients have never connected the dots, or have made the connection but assumed it was irrelevant because the infection resolved long ago. The history of a triggering illness is clinically important and sometimes missed.

Validate both phases. The acute phase was real. The persistent phase is also real. The transition between them does not require an ongoing pathogen to explain it. Framing persistence as central sensitization gives patients something accurate and non-dismissive to hold on to.

Be especially careful with Long COVID and Lyme. These communities have often felt dismissed, and in many cases, they have been. The nervous system framing is not an alternative to taking their experience seriously. It is a way of taking it seriously through a more complete lens. Introduce it as an additional explanation, not a replacement for their own understanding of what happened to them.

Prognosis matters. Post-infectious central sensitization can resolve. PRT and related approaches have shown meaningful outcomes in overlapping populations. The prognosis is not hopeless, and patients benefit from hearing that directly and specifically.

This Week on the Pain Reprocessing Therapy Podcast

When the Illness Ends but the Body Doesn’t Know It

Everything we described in this newsletter, the way a nervous system can stay activated long after an infection clears, the way symptoms persist without a pathogen to explain them, is a lot easier to understand when you hear it happening in real time.

In Season 2, Episode 3, host Daniel Lyman shares a recording from a real therapy session. His client, Eric, had been living with chronic fatigue for years. The symptoms began after mono. The infection resolved. The exhaustion did not.

Over seven weeks and eight session clips, you’ll hear what recovery actually looks like: not a single breakthrough moment, but a series of small shifts that gradually taught Eric’s nervous system that it was safe. By the end, he’s cycling, hiking, and back at work with clarity he hadn’t felt in years.

Listen to Season 2, Episode 3

Actions to Take After Reading This Newsletter

1. If your symptoms began after an illness, consider whether the post-infectious framework described here resonates with your experience. You are not obligated to find it persuasive. But if it opens something, that opening is worth following.

2. Notice whether your symptoms fluctuate with stress, sleep, or emotional state. That kind of variability is not evidence that your symptoms are imaginary. It is evidence that the nervous system is involved, which is useful clinical information, not a dismissal.

3. If you are a clinician, add a question about illness onset to your intake. Ask: Was there a period when you got sick and never fully recovered? The answer can change the direction of treatment.

4. Be cautious about the story you are carrying about what recovery is supposed to look like. Post-infectious fatigue and pain do not resolve on a predictable timeline, and comparing your progress to someone who did not experience sensitization is not a useful benchmark.

5. If you have been told your symptoms are anxiety or deconditioning without a full evaluation, consider seeking out a clinician who is familiar with central sensitization and post-infectious syndromes. The framework your provider uses shapes what they are able to offer you.

6. This week, listen to the PRT Podcast. Daniel Lyman sits down with a client whose chronic fatigue began with mono and works through in real time how the nervous system can hold onto symptoms long after the original illness has passed.

7. Share this newsletter with someone who has been struggling with symptoms since an illness and has not found answers. Sometimes the right framework is the thing that changes everything.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

What doesn’t get talked about enough is the quiet, heavy frustration experienced by those who are still stuck despite doing everything “right.” This isn’t the disappointment of someone who hasn’t tried. It’s the deep discouragement of someone who has left no stone unturned: reading every book, listening to every podcast, working with coaches, practicing somatic tracking, journaling, meditating, and diving into the neuroscience behind their pain. They show up, day after day, with hope and determination, only to feel like they’re spinning their wheels.

If that’s you right now, this one is for you, and know that you are not alone.

And if you’re a clinician who has ever sat across from a patient who is doing everything right and still not moving the needle, this one is for you, too.

The Missing Piece Isn’t More Effort

The crucial distinction in pain reprocessing is this: grasping the framework intellectually is not the same as experiencing real healing. You can study the neuroscience, understand the fear-avoidance loop, and know every step of PRT, yet still find yourself not progressing. The difference lies in how conditions support, or hinder, actual transformation.

This isn’t a failure of knowledge or effort. The nervous system doesn’t heal just because we understand it or will it to change. Healing happens when the nervous system feels safe enough to update its patterns, which requires more than just having good information. True change occurs in the right environment, at the right time, and sometimes with a willingness to shift focus away from fixing the symptoms altogether. It might mean tending to emotional needs, addressing life stressors, or slowing down to offer yourself compassion instead of pressure. It’s about creating a safe environment to facilitate healing and change, and then using PRT tools with an easy and effortless energy.

Ask yourself: does your environment support true change, or just more effort? Nurturing the right conditions, not pushing harder, is what allows healing to begin.

You Can’t Build Safety in an Unsafe Environment

A central principle of PRT is that the nervous system can only heal when it genuinely feels safe. Pain arises when the brain senses any kind of threat, whether physical, environmental, or psychological. To recover, the key is not just getting rid of the symptoms but creating an overall sense of safety in your body and mind, which helps deactivate the brain’s danger signals and ultimately turns off the pain.

A lot of people approach recovery the way they approach everything else in their lives, with intensity, discipline, and a drive to get it right. They do their somatic tracking every day. They journal. They show up to every session prepared. And somewhere in all of that effort, they forget that the nervous system isn’t grading their homework. It’s scanning the environment and asking one question: Am I safe right now?

If the answer coming back is no because of the way they are approaching their treatment, a relationship that’s draining them, a pace of life that never lets them exhale, a pattern of self-criticism that runs louder than any tool they’re using, then the work has nowhere to land.

Safety isn’t just a feeling to practice. It’s a condition to create.

Doing It “Badly” Is Part of Doing It

Many of my patients are driven, high-achieving individuals. Ironically, for people with lofty standards, the hardest part of recovery is often allowing themselves to do something imperfectly or incompletely. It can feel deeply uncomfortable, even threatening, to do an activity at a lower level than they once could, or to make progress that feels small.

But this is one of the most powerful and overlooked truths in recovery: growth happens when you practice new things imperfectly, slowly, and even uncertainly. Doing something at a fraction of your former capacity isn’t a sign of failure, it’s exactly how your brain and nervous system learn that it’s safe to try.

You can logically understand that bending over won’t harm your back, or remind yourself that a movement is safe. But your brain only truly believes it when you actually do the thing, live through it, and notice that nothing catastrophic happens. Lived experience is what rewires the brain’s threat system, not just intellectual knowledge.

So, the short walk around the block, even if you used to run marathons, counts. The session where your only progress is a shift in your affect or emotional state counts. Every imperfect attempt is a rehearsal for safety, building new neural pathways even when the results aren’t visible yet.

The real trap is dismissing these small steps as inadequate because they don’t match your old benchmarks. In truth, these incremental efforts are the work. Nervous system progress is rarely linear or dramatic, especially at first. It unfolds gradually, in the quiet space between the attempt and the realization that nothing bad happened.

This Is Not About Minimizing Your Pain

This is a hard one, because of course, it feels like the symptom is the problem. That’s the pain or fatigue that brings people into treatment in the first place. But when the entire focus of recovery is eliminating the symptom at all costs, something crucial is overlooked: the patterns, habits, and life conditions that set the stage for the symptom to emerge and persist. Plus, you send the message that the symptom is dangerous in the first place, and needs to be fixed.

If we only try to get rid of pain without examining and addressing those underlying patterns, it’s like turning off the check engine light without ever looking under the hood. The warning light disappears, but the real issue remains unresolved.

These patterns show up in subtle, everyday ways. There’s the person desperate to eliminate fatigue so they can return to working marathon hours without pause. Or the person who does somatic tracking and measures their success only by whether their pain score dropped, never noticing the mounting pressure or anxiety that surrounds their efforts. Or the person who does everything “right” in session, but then returns to a home or work environment that keeps their nervous system in a constant state of vigilance or stress.

The patterns are always part of the picture, even when they’re invisible at first. Sometimes, the most important clinical question isn’t “How is your pain today?” but “What does a normal Tuesday actually look like for you?” In other words, what are the rhythms, stressors, supports, and habits in your daily life that might be contributing to your pain?

To take it a step further, pain itself is not the problem to solve. Pain is your protector, your internal warning signal, and not an enemy to defeat. It exists to get your attention, signaling that something needs care or change, whether it’s a boundary being crossed, a personal need going unmet, an unresolved emotion, or chronic stress. The key is to listen to what the pain is communicating, rather than simply trying to silence or overpower it.

With neuroplastic pain, the focus is never to fix a physical injury or structural issue.

More often, it’s an unmet emotional need, a psychological tension, or an environment that keeps your nervous system on high alert. When you shift from asking “How do I make my pain go away?” to “What is my pain asking of me?” you open the door to true and lasting change.

Your Identity Might Be Holding On

There’s one more piece that doesn’t come up often enough, and it’s a little spicy: sometimes people are stuck because pain has become part of how they understand themselves.

This isn’t because anyone wants to be in pain. Not consciously. But when symptoms persist, they can begin to shape everything: what you do, what you avoid, how you relate to others, and even where you seek belonging. Pain becomes a lens through which you interpret your world, and like any lens, it can be difficult to remove, even when you’re ready for change.

Consider reflecting on this: Who might you be, and what would you do differently, if pain no longer defined your story? You don’t need to answer right away, but sitting with this question can be powerful. True recovery isn’t just about symptom reduction, but about building a life your nervous system genuinely desires to return to.

Actions to Take After Reading This Newsletter

Reflect on the difference between understanding pain intellectually and creating conditions for real healing in your environment.

Assess whether your current approach to recovery is based on pressure and effort, or on cultivating safety and self-compassion.

Identify areas of your life that might be keeping your nervous system in a state of threat, such as relationships, work pace, or self-critical habits.

Practice allowing yourself to do recovery activities imperfectly or incompletely, and notice any discomfort or resistance that arises.

Take note of small steps and imperfect attempts as valid progress, rather than dismissing them as inadequate.

Consider the underlying patterns, habits, or life circumstances that may be contributing to persistent symptoms, rather than focusing solely on eliminating pain.

Ask yourself: “What is my pain asking of me?” and explore what care or changes might be needed.

Reflect on how your identity may be shaped by living with pain, and imagine what might be different if pain no longer defined your story.

If you are a clinician, think about how you can help patients feel safer and supported in their environment, not just better informed.

Revisit your recovery tools and practices with an easy, gentle energy rather than intensity or urgency.

From the PRT Podcast

Season 2 of the PRT Podcast kicks off with a conversation that’s long overdue. New host Daniel Lyman, LCSW, Executive Director of the Mind Body Therapy Center, sits down with clinician Gabrielle Jacobs for “When the Work Isn’t Working: 5 Reasons You May Still Be Stuck,” digging into the reasons recovery stalls, even when people are doing everything “right.”

It’s honest, warm, and full of the kind of real clinical insight that only comes from practitioners who have actually been in the room with these moments. A great listen for patients and clinicians alike.

🎧 Listen now!

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

For some, particularly those with histories of childhood adversity, that something bigger is trauma.

Pain Reprocessing Therapy (PRT) is a two-pronged approach. The first prong addresses fear around the symptoms themselves, which refers to the responses and behaviors that fuel the pain. The second prong focuses on general fears that keep the nervous system on high alert, the layer underneath that contributes to a person’s lack of felt safety, keeping the pain active. Past trauma is one factor that can impact someone’s present sense of safety and relationship with fear, and deserves its own honest conversation.

The Nervous System Doesn’t Forget

To understand how trauma connects to chronic pain, it helps to start with the autonomic nervous system, the part of the nervous system that governs our threat response without us having to think much about it.

When we perceive danger, the sympathetic nervous system kicks in. Heart rate increases, muscles tense, and stress hormones flood the body, increasing our chances of survival. These automatic physiological responses are part of the fight-or-flight response, one of the most sophisticated protective mechanisms we have.

The problem is that the brain’s threat-detection system cannot distinguish between real and perceived danger. It responds to both with the same urgency. And for people who grew up in environments where danger was frequent, unpredictable, or chronic, that threat-detection system gets recalibrated. It learns, quite reasonably, that the world is less safe. So it stays on high alert. It scans constantly. And understandably, it finds threats more often.

Over time, this state of chronic activation, called sympathetic dominance, becomes the nervous system’s default setting. Stress hormones that are typically meant to spike and then recede remain constantly elevated. The body holds tension it can’t fully release, and the nervous system doesn’t rest and recover. That persistent state of arousal, that engine that never fully idles, creates the physiological conditions in which chronic pain can fairly easily take root and hold on.

This tendency and hyperarousal aren’t signs of weakness. It is the nervous system doing exactly what it was taught to do, protection and survival.

Where PRT and Trauma Overlap, and Where They Diverge

We conceptualize PRT as a framework that helps patients shift from an overall sense of danger to one of safety. To reiterate, the first prong of PRT works by helping the brain learn that pain signals are not dangerous, that the sensations can be observed with curiosity rather than fear, that the body is safe, and that the alarm can be turned down. For many people, this first prong is exactly what’s needed, and it works powerfully.

But for others, that second prong of working to increase overall felt safety is just as, if not more, important. For example, this work may include increasing self-care and self-compassion, examining current relationships, and creating boundaries. But for someone whose nervous system learned long ago that safety was rare or unreliable, the work of convincing the brain that it’s safe now can run into a deeper layer of resistance. PRT is still applicable, but the nervous system needs more than new information about pain, the first prong alone. It may need to do some direct work on its relationship with safety itself.

This is where trauma-informed approaches become relevant, not as a replacement for PRT, but as a companion to it. Approaches that work directly with the autonomic nervous system, helping it build the capacity to recognize safety in the present moment, release stored tension, and tolerate stillness without bracing, can lay the foundation for PRT, specifically that first prong, to be more available and more effective.

The Timing Question: Does Trauma Work Need to Come First?

This is one of the most common questions clinicians ask, and the honest answer is: it depends.

For some patients, addressing trauma directly before or alongside PRT is essential.

If the nervous system is so dysregulated that it can’t access a window of calm long enough to practice somatic tracking or engage curiously with sensations, the foundational work of regulation must come first. Trying to build safety in the body when the body has no reference point for safety is like trying to paint a wall that hasn’t been primed.

For others, PRT can begin right away, and the process of working with pain itself becomes part of the healing from trauma. Learning that the body can be approached with curiosity rather than braced against, that sensations don’t have to be emergencies, and that we have agency over how we respond are profoundly reparative experiences for someone whose history taught them the opposite. In these cases, PRT and trauma work aren’t sequential. They’re happening simultaneously, each reinforcing the other.

The clinical judgment call often comes down to one question: Does this person have enough access to a regulated state to do the work? If yes, you can begin PRT and fold in trauma-informed support as needed. If the nervous system is so chronically activated that regulation itself feels impossible, starting there first usually makes PRT techniques that much more effective when you get to it.

Neither path is wrong. The goal in both cases is the same: to help patients shift toward felt safety and for a nervous system to know it’s safe.

A Coping Skill from Our Community

This week’s coping skill comes from one of our readers, a certified trauma therapist who works with chronic neuroplastic pain. He shared a self-regulation approach drawn from the work of Dr. Eric Gentry, whose Forward Facing Trauma Therapy offers a practical, in-the-moment method for interrupting the fight-or-flight response.

What makes this approach stand out is that, once practiced, it can be done in seconds and integrated into daily life, rather than requiring a dedicated session or separate practice time.

It has three components:

Neuroception, establishing present-moment safety. When a threat is perceived, pause and ask: Am I in real danger right now? In most moments, the answer is no. Naming that, I am safe in this moment, interrupts the automatic fear response before it can escalate. This isn’t bypassing the feeling. It’s offering the nervous system accurate information.

Interoception, turning attention inward. Rather than staying focused on external stressors or anxious thoughts, shift attention to what’s actually happening in the body. Specifically, scan for muscle tension, the most reliable physical indicator that the fight-or-flight response has been triggered. The body is always giving information. The practice is learning to read it.

Acute relaxation, the full-body release. Dr. Gentry calls this the “wet noodle” exercise: a slow scan from head to toe, deliberately softening tense areas, neck, shoulders, jaw, stomach, pelvic floor, until the body feels limp and relaxed. This matters beyond comfort. As Dr. Gentry notes, it is physiologically impossible to be in a fight-or-flight response when the muscles are relaxed. Releasing the tension isn’t just soothing. It’s directly interrupting the stress response at the level of the body.

One important note for clinicians: patients with significant childhood trauma histories may experience somatic dissociation, a difficulty connecting with bodily sensations that makes interoception harder. This is normal, not a failure. With patience and practice, that awareness can be developed. Meeting patients where they are with this skill, rather than expecting immediate fluency, is part of what makes it effective over time.

PRT Research

The link between adverse childhood experiences and chronic pain is well-documented. The landmark ACE (Adverse Childhood Experiences) study found a strong correlation between the number of childhood adversities a person experienced and their likelihood of developing chronic pain and other health conditions in adulthood. Simply put, the more difficult experiences someone has early in life, the greater their chances of developing chronic pain and other health problems later on. This pattern shows just how much our ongoing stress and nervous system responses can shape our physical well-being.

A recent study in The Journal of Pain (Tankha et al., 2023) shared what many people experience firsthand: patients naturally talked about their emotions in PRT sessions, especially those connected to trauma or difficult life events, even if it wasn’t the main goal. Clinicians who listened to and responded to their patients’ needs found that these honest emotional conversations often played an important role in helping people find relief from pain.

This suggests that for many patients, the line between pain work and trauma work isn’t as clean as a treatment protocol might imply. They are often working on the same thing from different angles.

Felitti VJ, et al. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. American Journal of Preventive Medicine. 1998;14(4):245–258.

Tankha H, Lumley MA, Gordon A, et al. “I don’t have chronic back pain anymore”: patient experiences in pain reprocessing therapy for chronic back pain. J Pain. 2023;24(9):1582–1593.

Actions to Take After Reading This Newsletter

Reflect on whether your history, or your patient’s history, might be a factor in how the nervous system is responding to pain treatment, without judgment or blame.

Consider whether the nervous system has enough access to a regulated state to engage with PRT tools, or whether foundational regulation work might be a helpful starting point.

Notice moments throughout the day when your body is holding tension, and practice the three-step self-regulation approach from this week’s coping skill: name your safety, check in with your body, and release.

If you are a patient, ask yourself honestly: does my daily environment, my relationships, my pace, my self-talk, support the nervous system in feeling safe? What is one small thing that could shift?

If you are a clinician, consider how trauma-informed awareness might enrich your PRT work, not by adding more to your sessions, but by staying curious about what your patient’s nervous system might be carrying beneath the pain.

Practice the “wet noodle” exercise once today, even for 60 seconds, and notice what changes.

Remember that healing trauma and healing pain are often the same work, approached from different doors. You do not have to choose one over the other.

Actively practice grounding: feel your feet on the ground, your seat in the chair, or the wind on your face. Simply notice sensations in the present moment.

Go outside. It resets the nervous system. Spending even five minutes outside reduces cortisol, lowers blood pressure, and decreases muscle tension.

Reading Corner: They Can’t Find Anything Wrong by Dr. David Clarke

Dr. David Clarke, a board-certified physician in internal medicine and gastroenterology, has worked with thousands of patients whose chronic symptoms had no clear medical explanation. In this book, he shares patient stories that reveal how hidden stress and trauma can drive persistent pain even when medical tests come back “normal.”

Dr. Clarke blends medical insight with compassionate storytelling, showing how uncovering and addressing underlying stressors can bring real relief. For patients, it offers hope and validation. For practitioners, it provides a deeper understanding of the mind-body connection and practical ways to support recovery.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

Clinicians working in this space knew the difference. The pain is real. The brain is real. The mechanism is real and measurable. But the science needed time to build the kind of evidence base that would make that conversation easier to have, and that the broader medical world would take seriously.

That time is here.

Where We Were

For most of modern medicine’s history, chronic pain has been understood primarily as a body problem.

Something is damaged, inflamed, compressed, or degenerating, and the treatment is to fix, remove, or manage that physical cause. When scans and tests came back normal, patients were often left without answers, or abruptly handed off to psychiatry with the implication that their pain might be emotional rather than real.

The psychological and neurological underpinnings of chronic pain were understood by researchers decades before they made it into clinical practice. The science of how the brain generates and amplifies pain, through learned neural pathways, threat detection systems gone into overdrive, and a nervous system that never quite got the message that the danger had passed, was there. But translating it into rigorous clinical evidence, the kind that gets published in major journals and taught in medical schools, takes time. It takes randomized controlled trials, fMRI studies, long-term follow-up data, and the courage of researchers willing to work at the edges of what medicine considers legitimate.

That work has been happening. And it is now arriving all at once.

What the Research Is Showing

The Boulder Back Pain Study, Five Years Later

The 2021 landmark study by Dr. Yoni Ashar and colleagues established Pain Reprocessing Therapy as the most effective current treatment for primary chronic back pain, with 66% of PRT participants pain-free or nearly pain-free after just four weeks, a result that made headlines across the medical community.

What is less widely known is that in July 2025, the same research team published five-year follow-up data in JAMA Psychiatry. More than half of those who received PRT were still nearly or completely pain-free five years later, continuing to outperform both the placebo and usual care groups. This kind of long-term durability data is rare in chronic pain research. It is not an exaggeration to say it changes what we know is possible.

Ashar YK, Low EL, Knight K, et al. Pain reprocessing therapy vs placebo and usual care for patients with chronic back pain: 5-year follow-up of a randomized clinical trial. JAMA Psychiatry. 2025;82(10):1049–1051.

EAET Is Outperforming the Gold Standard

Emotional Awareness and Expression Therapy, which shares roots with PRT in its emphasis on the brain’s role in generating pain and the importance of emotional processing, has been quietly building a remarkable evidence base of its own.

A 2024 randomized clinical trial published in JAMA Network Open compared EAET to cognitive behavioral therapy, long considered the gold standard psychological treatment for chronic pain, in a diverse group of 126 older veterans with musculoskeletal pain. EAET produced significantly greater pain reduction.

Notably, 63% of EAET participants achieved clinically significant pain reduction compared to only 17% in the CBT group. These are not incremental differences. They are the kind of results that shift how a field thinks about what treatment should look like.

Yarns BC, Jackson NJ, Alas A, et al. Emotional awareness and expression therapy vs cognitive behavioral therapy for chronic pain in older veterans: a randomized clinical trial. JAMA Network Open. 2024;7(6):e2415842.

Multisensory Sensitivity as a Marker of Neuroplastic Pain

One of the more fascinating emerging areas of research involves multisensory sensitivity, the tendency of people with chronic pain to also be sensitive to bright lights, loud noises, certain textures, and other everyday sensory inputs that most people don’t notice. A growing body of evidence suggests this widespread sensory amplification may be a meaningful indicator of altered central nervous system processing, in other words, a signal that the brain’s threat system has become broadly sensitized, not just in the pain system, but across the senses.

This research matters because it offers a new window into understanding who is experiencing neuroplastic pain and why, and it opens new possibilities for how we assess and tailor treatment. When a patient mentions they are also bothered by fluorescent lights and certain fabrics, that is not necessarily a separate issue from their pain. It may be the same system expressing itself in multiple ways.

Dunne H, Frey-Law LA. Multisensory sensitivity in relation to pain: a scoping review of terminology and assessment. Pain Rep. 2024 Oct 25;9(6):e1193. doi: 10.1097/PR9.0000000000001193. PMID: 39473878; PMCID: PMC11519410.

Migraines: A Small Case Study

A very small case series revealed strong results on the efficacy of PRT for headaches and migraines. Patients experiencing an average of 25 to 30 headaches or migraines per month underwent PRT sessions and lowered symptom frequency to only 3 to 5 headache or migraine days per month. Sessions focused mainly on education about neuroplastic pain and its relevance to migraine as well as guided instruction of somatic tracking. These pain sufferers experienced large reductions in symptom frequency, meaningful improvements in pain intensity and functional outcomes, and healing of comorbid pain symptoms.

Fishbein JN, Schuster NM, Anders A, Portera AM, Herbert MS. Pain Reprocessing Therapy for migraine: A case series. Headache. 2025;65:1660-1665. doi:10.1111/head.15043

Women’s Health: Chronic Pelvic Pain, Psychiatric Diagnoses, and Sexual Abuse

Two groups of women underwent laparoscopy, one group had chronic pelvic pain, the other did not. Interestingly, structural findings did not differ among symptomatic versus asymptomatic patients, with no significant differences found in degree or type of pelvic disease or the prevalence of endometriosis. However, the symptomatic patients had a significantly greater prevalence of major depression, lifetime substance abuse, and were three times more likely to have been a victim of childhood or adult sexual abuse.

With these findings, we cannot ignore the brain’s role in pain, taking patients’ trauma histories into account.

Harrop-Griffiths J, Katon W, Walker E, Holm L, Russo J, Hickok L. The association between chronic pelvic pain, psychiatric diagnoses, and childhood sexual abuse. Obstet Gynecol. 1988 Apr;71(4):589-94. PMID: 2965326.

Normal “Abnormalities” on MRI

In a cross-sectional study of 602 adults aged 41-76, 99% had at least one rotator cuff abnormality such as tendinopathy, partial tears, or full-thickness tears. Importantly, abnormalities were present regardless of pain. 96% of pain-free shoulders had abnormalities while 98% of painful shoulders had abnormalities. Many full-thickness tears occurred in people with no symptoms, and findings increased with age.

So, in most cases, structural findings do not reliably explain pain and should not guide diagnosis or treatment alone.

In a similar vein, a study found 98% of 222 patients with chronic low back pain had at least one abnormality on MRI. But when researchers examined symptom patterns, stressors, and variability in pain, 88% were found to have nonstructural pain.

Ibounig T, Järvinen TLN, Raatikainen S, et al. Incidental Rotator Cuff Abnormalities on Magnetic Resonance Imaging. JAMA Intern Med. 2026;186(4):406–414. doi:10.1001/jamainternmed.2025.7903

Schubiner H, Lowry WJ, Heule M, Ashar YK, Lim M, Mekaru S, Kitts T, Lumley MA. Application of a Clinical Approach to Diagnosing Primary Pain: Prevalence and Correlates of Primary Back and Neck Pain in a Community Physiatry Clinic. J Pain. 2024 Mar;25(3):672-681. doi: 10.1016/j.jpain.2023.09.019. Epub 2023 Sep 28. PMID: 37777033.

What This Means for Patients

If you have been on this journey for a while, doing the work, learning the science, sitting with the frustration of a medical system that didn’t have language for what you were experiencing, this moment in research is worth pausing to acknowledge.

The science has caught up.

What you have been told about your pain, that it is real, that it is being generated by a brain in protection mode, and that it can change, is now supported by a growing body of rigorous, peer-reviewed, published evidence.

The results are not modest or preliminary. They are significant and, in some cases, durable for years.

You were not wrong to believe in this. And the path forward has never been more clearly marked.

What This Means for Clinicians

The evidence base you have been waiting for, the kind that lets you walk into a referral conversation or a skeptical colleague’s office and cite published data, is here and it is growing. These findings are not fringe. They are being published in the same journals where medicine takes its cues.

That matters not just for your patients, but for the field. Every practitioner working in this space is part of a paradigm shift that is now well underway. The research is validating what skilled clinicians have been observing for years. The question now is how quickly the broader medical system catches up, and how many people reach effective treatment before it does.

Actions to Take After Reading This Newsletter

If you are a patient, let the weight of this research land. You are being treated with an approach that is now backed by some of the strongest evidence in chronic pain medicine.

If you are a clinician, identify one conversation with a colleague or referral source where this research would be useful, and bring it.

Stay up to date with the latest publications via our Instagram, @painreprocessingtherapy.

Find even more research on neuroplastic symptoms via the ATNS.

Share this newsletter with someone who needs to hear that the science has caught up, a patient who has felt dismissed, a colleague who is curious, or someone who is still searching for answers.

Take a moment to notice what it means to be on the right side of a paradigm shift that is now well underway.

If you are a clinician and want to bring this research into your sessions right away, the PRT Practitioner Media Guide gives you the language, scripts, analogies, and tools to translate the science into conversations your patients can understand. It’s a pull-it-off-the-shelf reference built for exactly this kind of moment. You can get the Media Guide here.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

“Consider structural and physiologic conditions with an overlay, or I suppose underlay, of brain influences, such as hypervigilance and trauma history. Can PRT be helpful even in the setting of known health conditions?”

The conversation around neuroplastic pain has done a tremendous amount of good.

It has given people language for experiences that were previously dismissed, validated suffering that the medical system couldn’t explain, and opened doors to treatments that have genuinely changed lives.

But somewhere along the way, a false binary has taken hold in some corners of the mind-body world: either your pain is structural, or it’s neuroplastic. Either the body is the problem, or the brain is.

For a significant number of people, that framing doesn’t fit. And when the framing doesn’t fit, people fall through the cracks.

Understanding Mixed Pain

Many patients do have truly neuroplastic conditions. But pain doesn’t always live in a single category.

The experience of pain is always a product of the brain. Even pain from clear structural causes must be processed, interpreted, and signaled by the nervous system before it becomes a felt experience. What this means in practice is that even when there is a genuine physical source of pain, the brain’s threat system is always part of the equation.

For people with known health conditions, rheumatoid arthritis, multiple sclerosis, cancer, Parkinson’s disease, ALS, and others, the structural component should not be dismissed or minimized. These conditions deserve proper medical management.

And yet, research consistently shows that the degree of structural damage does not reliably predict the degree of pain or disability. Two people with identical imaging findings can have dramatically different pain experiences. A person with minimal visible inflammation can be debilitated. Another with significant joint damage may function with relative ease.

The structural finding alone does not tell the whole story.

That gap, between what the body shows and what the person experiences, is where the nervous system lives.

The Amplifier Problem

When the body is dealing with a chronic health condition, the nervous system is receiving a steady stream of incoming signals. Over time, particularly when that input is persistent, unpredictable, or accompanied by fear, the brain’s threat-detection system can become broadly sensitized.

It lowers its threshold.

It starts responding more intensely to signals that would otherwise pass without much notice.

And crucially, it begins generating pain not just in response to the actual physical source, but in anticipation of it, in response to movement that was once feared, and in reaction to stress, fatigue, and emotional distress that have nothing to do with the structural condition itself.

This process is called central sensitization, and it has been documented across a wide range of conditions including fibromyalgia, osteoarthritis, rheumatoid arthritis, Ehlers-Danlos syndrome, upper extremity tendinopathies, headache disorders, and back pain.

A comprehensive review published in The Lancet Rheumatology found central sensitization present across all of these conditions, often in a subset of patients whose pain was disproportionate to the degree of structural damage or inflammatory activity.

In rheumatoid arthritis specifically, nearly a third of patients also meet criteria for fibromyalgia syndrome, a pattern that reflects not just one condition but a nervous system that has become broadly amplified.

Centralization of pain can occur when peripheral nociceptive input persists over time, creating what researchers describe as a mixed pain state, one in which structural and centrally amplified pain coexist and interact.

Recognizing and addressing the central component is associated with improved outcomes even when the peripheral condition remains.

What this means is that for many people with known pathology, there are two simultaneous processes happening.

There is the underlying structural or inflammatory condition, producing real signals.

And there is a sensitized nervous system amplifying those signals, generating fear around them, and sometimes producing pain independently of the structural source entirely.

Treating only one of these while ignoring the other leaves a significant part of the problem unaddressed.

Nijs J, George SZ, Clauw DJ, et al. Central sensitisation in chronic pain conditions: latest discoveries and their potential for precision medicine. Lancet Rheumatol. 2021;3(5).

Where PRT Fits In

PRT was developed with primary neuroplastic pain as its focus, pain that exists in the absence of structural damage, or that persists long after an injury has healed.

And it is most clearly indicated in those cases.

But the principles that make PRT effective do not stop applying the moment a structural diagnosis enters the picture.

The fear-avoidance cycle is just as active in someone with osteoarthritis as in someone with no structural findings.

The tendency to brace against movement, scan for danger, and interpret every sensation as a warning of damage amplifies pain regardless of whether there is an underlying condition driving the signal.

And trauma history, hypervigilance, and a nervous system chronically oriented toward threat make everything harder, regardless of what the imaging shows.

For these patients, PRT and related approaches may not eliminate the underlying condition or fully resolve the structural pain.

But they can meaningfully reduce the amplification that sits on top of it.

They can help the nervous system distinguish between the signal that genuinely needs attention and the alarm that has grown beyond proportion.

They can give patients agency over a part of their experience that medical management alone cannot touch.

This is not a consolation prize.

For someone whose pain has tripled because their nervous system is in overdrive on top of a physical condition, bringing that amplification down is profoundly meaningful.

It may not be the same outcome as full recovery from primary pain, and it should not be framed as such.

But it is real, it is achievable, and it is worth pursuing.

Plus, Normal Abnormalities Exist

It is also worth remembering that asymptomatic people are not free of physical findings.

Studies show that an average of 87% of asymptomatic adults have bulging discs in the neck. Seventy-two percent have superior labral tears in the shoulders. Sixty-nine percent, and 89% of athletes, have labral tears in the hips. Sixty-three percent have Achilles tendon changes. Sixty-eight percent of runners have retrocalcaneal changes. And 97% of knees show some abnormalities.

Disc degeneration in the back exists in 52% of asymptomatic people in their 30s and rises to 96% of asymptomatic people in their 80s.

These numbers are incredibly significant because they remind us that findings on imaging do not automatically explain symptoms.

Brinjikji et al. Systematic literature review of imaging features of spinal degeneration in asymptomatic populations. AJNR Am J Neuroradiol. 2015 Apr;36(4):811-6.

What This Looks Like Clinically

For healthcare providers working with patients who have known structural conditions, the key shift is this:

Stop treating the structural diagnosis as the end of the story.

When a patient with rheumatoid arthritis describes pain that fluctuates wildly, spreads beyond the affected joints, worsens with stress, or feels entirely out of proportion to their current inflammatory markers, that is a signal worth attending to.

When a patient with degenerative disc disease avoids movement so thoroughly that their world has shrunk around the pain, the fear is part of the picture.

When someone with a known condition also carries a history of trauma, childhood adversity, or chronic hypervigilance, those nervous system patterns are shaping their pain experience in real time.

The clinical question is not whether the structural condition is real. It is.

The question is how much of what this patient is experiencing is being amplified by a sensitized nervous system, and what can be done about that layer specifically.

In many cases, the answer is quite a lot.

Some Practical Considerations

Set clear, honest expectations. PRT approaches can reduce amplification and improve quality of life, but they will not cure an underlying condition.

Start with validation. Patients with known conditions are often particularly sensitive to any implication that their pain is not real because they have spent years fighting to receive a diagnosis or have their diagnosis taken seriously.

Work with what moves. Even in patients with structural conditions, looking for signs of neuroplastic overlay, pain that fluctuates independently of physical activity, spreads beyond the structural site, or responds strongly to emotional states, provides useful clinical entry points.

Hold both simultaneously. Medical management of the structural condition and nervous system work are not in competition. They address different layers of the same experience, and patients do better when they do not have to choose.

What This Means for Patients

If you are living with a known health condition and have been told, explicitly or implicitly, that the mind-body approach is not really for you, we want to be clear:

That is not accurate.

PRT may not be able to treat you completely.

But a nervous system in a state of chronic amplification, shaped by fear, bodily preoccupation, trauma, and years of bracing for pain, is something that can change, even when the structural picture is complicated.

You do not have to have “pure” primary pain to benefit from approaches that calm the threat system, reduce fear around movement, and help your nervous system learn that not every signal is an emergency.

In fact, the worst-case scenario is a better quality of life and movement toward felt safety in your everyday life, even if the pain itself is not touched.

Your pain is real.

Your diagnosis is real.

And the amplification sitting on top of it is also real, and it is addressable.

Reading Corner

[INSERT: Reading Corner Image]

The Mindful Body: Thinking Our Way to Chronic Health
Ellen J. Langer

What matters more, the mind or the body?

The Mindful Body is a social psychologist’s view on the healing power of the mind, demonstrating how our thoughts and perspectives have the potential to profoundly shape our well-being.

This book will leave you with compelling evidence that our thoughts influence the state of our bodies, for better and for worse.

If you are ready for a paradigm-shifting read, pick up a copy and let us know what you think!

Get Support That Holds the Whole Picture

If you’re living with a known health condition and chronic pain, you deserve care that takes both seriously.

WellBody therapists understand the complexity of mixed pain and are trained to work with the nervous system layer alongside your medical treatment.

Whether you’re navigating autoimmune conditions, hypermobility, chronic pain, or symptoms that seem larger than the structural picture alone can explain, you don’t have to figure it out by yourself.

[BUTTON: Connect with a WellBody Therapist → https://getwellbody.com/schedule-an-intake]

Actions to Take After Reading This Newsletter

1. If you have a diagnosis and have assumed that PRT or mind-body approaches are not for you, consider whether central sensitization or nervous system amplification might be part of your experience, even alongside a structural finding.

2. Notice whether your pain fluctuates in ways that do not track with your structural condition, lighter on vacation, heavier during stress, spreading beyond its usual location, or being triggered by certain movements sometimes but not always.

3. If you are a clinician, ask patients with structural diagnoses how their pain varies and what makes it better or worse beyond their medical management. The answers often reveal a nervous system component waiting to be addressed.

4. Hold the complexity. You do not have to choose between your diagnosis and a brain-based approach. Both layers can be true, and both deserve care.

5. Know that a structural finding is not the be-all and end-all. In some cases, a finding may be completely unrelated to your pain experience.

6. If the amplification layer is a significant part of your pain experience, consider exploring PRT approaches, not as a replacement for medical treatment, but as a meaningful complement to it.

7. Share this newsletter with someone who has been told there is no hope for pain improvement. This conversation needs to be broader than it has been.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

“Chronic pain in neurodivergent populations? It seems to be understood that there are links between chronic pain and neurodiversity, and that joint hypermobility and autoimmune disorders are common to these groups too.”

She shared that she has experienced neuroplastic pain for years, was diagnosed with ADHD later in life, and has several autoimmune conditions. She also noted that many people she has met in chronic pain groups seem to be in the same boat.

She’s right. And she named something that the traditional mind-body community has been slow to address. This week, we want to start that conversation.

The Overlap Is Not a Coincidence

If you spend time in chronic pain communities, you may notice that a disproportionate number of people there also identify as neurodivergent. For a long time, this was treated as coincidence, or dismissed as the result of neurodivergent people simply being more attuned to their bodies and therefore more likely to report symptoms.

But the research tells a different story.

Early research suggests the overlap is significant. A 2026 case-control study found that among patients with chronic pain and chronic fatigue, those with chronic pain were approximately 14 times more likely to meet criteria for autism and nearly 13 times more likely to meet criteria for ADHD compared to a non-clinical group. Yet only around 8% had a prior autism diagnosis and 7% had a prior ADHD diagnosis.

The gap between who may have these conditions and who has been identified is striking, and points to something important: a significant number of people navigating chronic pain may be doing so with a nervous system that was wired differently from the start, often without knowing it.

Quadt L, Savage G, Bond R, et al. Likely neurodivergence and variant connective tissue in patients with chronic pain/chronic fatigue: a case-control study. J Psychiatr Res. 2026.

What Neurodivergence and Chronic Pain Have in Common

The connection between neurodivergence and chronic pain is not simply that neurodivergent people experience more pain. It runs deeper than that into shared neurological mechanisms that intertwine the two conditions.

Central sensitization, the process by which the brain’s threat-detection system becomes broadly sensitized, producing pain in response to signals that would otherwise pass unnoticed, appears to be significantly more common in both autistic people and those with ADHD. A 2022 study published in Molecular Autism found that 21% of a large sample of autistic adults had been diagnosed with a central sensitivity syndrome, but over 60% met the criteria for one, conditions including fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, restless leg syndrome, and migraines.

And in a follow-up study, participants with a diagnosed central sensitivity syndrome also reported more autistic traits than those without the diagnosis, suggesting the relationship runs in both directions.

But once researchers accounted for sensory sensitivity and anxiety, the association changed. Meaning, the overlap between autistic traits and central sensitivity symptoms may be largely driven by factors of sensory sensitivity and anxiety, rather than a direct autism-to-chronic-pain pathway.

Research also suggests some neural circuits involved in attention, salience detection, emotion, interoception, motivation, and pain overlap in ADHD, including the anterior cingulate cortex and insula. This may help explain why people with ADHD also experience higher rates of chronic pain, sensory sensitivity, or emotional dysregulation.

Grant S, Norton S, Weiland RF, Scheeren AM, Begeer S, Hoekstra RA. Autism and chronic ill health: an observational study of symptoms and diagnoses of central sensitivity syndromes in autistic adults. Molecular Autism. 2022;13(1):7.

Firouzabadi FD, et al. Neuroimaging in ADHD. 2022.

Multi-Sensory Sensitization

Multi-Sensory Sensitization (MSS), also referred to as multi-sensory hypersensitivity or hyperresponsivity, is heightened reactivity to stimuli beyond pain, like sounds, sights, and smells. When it comes to chronic pain, the brains of those with MSS will not only amplify pain sensations, but all sensory input.

People high on the MSS scale are 2 to 3.5 times more likely to report chronic pain.

Interestingly, data shows that perceived brightness to a light source predicts response to surgery. Meaning, the brighter the light seemed, the more likely that person was to not respond to surgery. Patients with chronic hip pain who reported the light as very bright were less likely to respond to hip replacement surgery, while patients with chronic pelvic pain who reported the light as very bright were less likely to respond to a hysterectomy.

In the same vein, chronic back pain patients exposed to unpleasant sounds found them significantly more distressing than healthy controls, both through self-report and brain imaging.

From these outcomes, we can consider a centralized volume knob on sensory amplification in the brain, amplifying all incoming stimuli: light, pain, sound, and more.

Nijs et al. 2023; Blomhoff et al. 2000; Dixon et al. 2016; Wilbarger et al. 2011; Harte et al. 2016; Kmiecik et al. 2022; Geisser et al. 2008; López-Solà et al. 2014, 2017; Waller et al. 2025.

The Hypermobility Thread

Another piece of this picture is joint hypermobility.

Research suggests that autistic people and those with ADHD are overrepresented in conditions like hypermobile Ehlers-Danlos syndrome and hypermobility spectrum disorders. These conditions involve connective tissue differences that produce joint instability, pain, fatigue, and dysautonomia, alongside a nervous system that is frequently sensitized.

The 2026 case-control study mentioned above found that joint hypermobility mediated the relationship between neurodivergence and the presence of chronic pain and fatigue, meaning hypermobility was a significant pathway through which neurodivergence contributed to these conditions.

For clinicians, this is a meaningful clinical signal. When a patient presents with chronic pain and hypermobility, asking about neurodivergence is not a detour. It may be central to understanding their full picture.

For patients, it means that if you are neurodivergent and hypermobile and in pain, these conditions are often associated and may share overlapping mechanisms, and that connection deserves to be named and treated as part of a coherent picture, not three separate problems requiring three separate specialists.

Why This Population Is Frequently Missed

There are several reasons why neurodivergent people with chronic pain often fall through the cracks of both systems.

First, the diagnostic gap is significant. As the 2026 study found, the majority of neurodivergent people in chronic pain settings had never been identified as such.

Second, there is a tendency in clinical settings to attribute neurodevelopmental traits to somatic symptoms rather than considering them independently.

Third, neurodivergent nervous systems often respond differently to standard therapeutic approaches. Sensory differences, interoceptive challenges, difficulty with emotional identification, and different communication styles can all affect how someone engages with somatic work, therapeutic relationships, and the tools that are central to PRT.

This does not mean PRT does not apply. It often applies powerfully. It means that adaptation, flexibility, and genuine attunement to how this person’s nervous system works are essential.

What This Means for Clinicians

Working with neurodivergent patients in chronic pain requires holding more complexity than the standard model always accounts for.

Some things worth considering:

• Screening matters.

• Interoception looks different.

• The threat system may have been on high alert for a long time.

• Language and pacing matter more than usual.

Neurodivergent patients often appreciate directness, clarity, and predictability in a therapeutic relationship.

The therapeutic tools of PRT remain relevant. The delivery may need to flex.

What This Means for Patients

If you are neurodivergent and in pain, and you have felt like the resources available to you were not quite built with you in mind, that feeling is valid.

But the core of what PRT offers, a nervous system that learns it is safe, a brain that is taught to interpret signals differently, a relationship between attention and sensation that can be changed, applies to you.

The biology is the same, even if the pathway to recovery may look different.

You are not too complicated for this work. Your nervous system is not too unusual for recovery. And the fact that your brain is wired differently does not mean it cannot unlearn danger and relearn safety.

Kilic O. Intersecting paths: exploring the link between neurodevelopmental disorders and chronic pain. Eur Psychiatry. 2025.

Quadt L, Savage G, Bond R, et al. Likely neurodivergence and variant connective tissue in patients with chronic pain/chronic fatigue: a case-control study. J Psychiatr Res. 2026.

Grant A, et al. Autism and chronic ill health: an observational study of symptoms and diagnoses of central sensitivity syndromes in autistic adults. Mol Autism. 2022;13(1):9.

Actions to Take After Reading This Newsletter

1. If you are neurodivergent and have chronic pain, consider whether the overlap described here resonates with your experience, and whether any of the pieces, hypermobility, central sensitization, or late diagnosis, might be worth exploring further with your care team.

2. If you are a clinician, ask yourself how often you screen for neurodivergence in your chronic pain patients. The diagnostic gap is significant, and the clinical implications are real.

3. If you work with patients who have sensory differences, consider how your somatic tools may need to be adapted, not abandoned, but approached with more flexibility and explicit scaffolding.

4. Share this newsletter with a colleague or patient who might not have connected these dots yet. This conversation needs to reach more people.

5. If this resonated with you personally, know that the complexity of your nervous system is not an obstacle to recovery. It is simply the landscape you are working in, and you can navigate it with the right support.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

This is not a fringe belief. It is one of the most consistently reported experiences across nearly every chronic pain condition, including arthritis, fibromyalgia, migraines, back pain, and CRPS. Patients bring it up unprompted, and many have tracked it over years. They are certain that the weather is causing these changes.

The symptoms are real. Something is happening. The question is what.

The Conventional Explanation (and Why It’s Incomplete)

The most common explanation for weather-related pain is barometric pressure. The theory is that when atmospheric pressure drops before a storm, tissues expand slightly, putting more pressure on sensitive joints and nerves. There is some research to support a small direct effect, but it cannot account for what people actually describe.

If barometric pressure were the primary driver for the significant increase in symptoms, we would expect the relationship to be consistent, predictable, and roughly proportional across those with similar conditions. That is not the case. Some people with severe arthritis report no weather sensitivity at all, while others with mild inflammation are completely derailed when the temperature drops. The same person may feel fine in damp Seattle and miserable in dry Colorado, or the reverse. The pressure-tissue theory does not explain that variability.

What it also does not explain is why the pain often arrives before the weather changes, and why so many people report feeling the storm coming hours before any measurable shift in pressure. The body, it turns out, is not just responding to the weather. It is anticipating it.

The Real Mechanism: Conditioning

In the early twentieth century, Ivan Pavlov demonstrated something that has shaped our understanding of the nervous system. He discovered that a dog can learn to associate a ringing bell with food, and eventually begin to salivate at the sound of the bell alone, even when no food follows. The bell becomes a signal, and the body responds to the signal as if the thing it predicts is already happening.

The nervous system does this constantly, with everything. It is not a flaw but an important evolutionary skill. The brain is a prediction machine. It learns from experience, builds associations, and fires responses in anticipation of what it has learned to expect. This is efficient. This keeps us alive. And in the context of chronic pain, this is exactly what happens with weather.

Here is how it tends to develop. At some point, often during a painful flare, the weather happened to be cold, or damp, or stormy. The nervous system, already sensitized and scanning for threat, logged that association. Cold equals danger. Rain equals pain. Over time, through repetition, that association strengthens. The brain does not wait to see how the weather will affect the tissues. It fires the pain signal when it detects the cue. The drop in temperature. The shift in light. The smell of rain. Because that is what it has learned to do. The pain is real. The mechanism is conditioning.

This reframe is not about telling people their weather sensitivity is imaginary. It is about offering a more accurate explanation for something that is genuinely happening. And unlike the pressure-tissue theory, this one opens a door: conditioned responses can change.

The science on weather and pain has produced some genuinely surprising findings. In a landmark study, researchers David Redelmeier and Amos Tversky recruited patients with chronic arthritis who believed strongly that weather affected their pain. Over an extended period, they tracked both patients’ daily pain ratings and the actual weather conditions. They found no statistically significant correlation between the weather and the patients’ pain. None. Yet every patient remained convinced the relationship was real.

This is not evidence that the patients were wrong to trust their experience. It is evidence that the nervous system is extraordinarily good at finding patterns, especially patterns it has been primed to find. The brain notices and remembers the days when weather and pain coincide. It does not register the misses in the same way. The association feels airtight because the nervous system built it to feel that way.

More recent research has found small but real correlations between certain weather variables and pain, particularly humidity and temperature, in large-scale studies using smartphone tracking data. The “Cloudy with a Chance of Pain” study out of the University of Manchester followed thousands of people with chronic pain conditions over several months and found that higher humidity, lower pressure, and stronger wind were associated with increased pain the following day. Real, but small. Far smaller than what patients typically report experiencing.

The gap between the small measured effect and the large felt experience is exactly where conditioning lives.

Redelmeier DA, Tversky A. On the belief that arthritis pain is related to the weather. Proc Natl Acad Sci. 1996;93(7):2895–2896.

Dixon WG, Beukenhorst AL, Yimer BB, et al. How the weather affects the pain of citizen scientists using a smartphone app. NPJ Digit Med. 2019;2:105.

Seasonal Affect: The Summer Effect

There is another layer to the weather-pain story that deserves its own space. Many people with chronic pain report that their symptoms genuinely improve in summer. Not just slightly, but meaningfully. They feel more like themselves, have more energy, and can do things that winter made impossible. And then October arrives, and the slide begins again.

Part of this is conditioning, running in reverse. Summer is associated with activity, warmth, freedom, and feeling well. The nervous system has learned those associations, too, and it responds to summer cues by loosening vigilance. But there is something else at play: the increase in light.

Light exposure is one of the most powerful regulators of the nervous system. Sunlight triggers serotonin production, which supports mood, pain modulation, and a general sense of safety in the body. It also regulates cortisol timing, helping the body maintain the morning cortisol peak that buffers inflammation, the same peak that drops in winter when mornings are dark. Seasonal affective disorder, which affects millions of people, is driven in significant part by this disruption in light-regulated neurochemistry. And many of its symptoms, low mood, fatigue, body heaviness, and pain sensitivity, overlap substantially with what people with chronic pain experience in winter.

This is not a coincidence. The nervous system that modulates mood and the nervous system that modulates pain are not separate systems. When light deprivation suppresses serotonin and disrupts cortisol rhythms, the pain modulatory system loses some of its buffering capacity. The body becomes more reactive, more sensitized, more prone to interpreting signals as threatening. Winter does not cause chronic pain, but it can turn up the volume on a nervous system that is already on high alert.

Some of what people experience as winter pain is the nervous system losing its seasonal footing. More light, more movement, less threat. These are not just comfort measures. They are biological ones.

What This Means for PRT

If conditioning substantially drives weather-related pain, then the treatment question is not how do we change the weather, but how do we change the association. And that is something Pain Reprocessing Therapy is specifically built to do.

The first step is naming what is actually happening. For patients who have spent years believing their winter pain means something is structurally wrong, understanding that the nervous system learned this pattern changes everything. When they understand that the brain generates pain based on its interpretation of threat rather than actual weather data, the threat loses some of its power.

From there, the PRT work involves approaching weather-triggered symptoms with curiosity rather than dread. The conditioned response runs on the expectation that when it gets cold, pain follows, confirming that cold means pain, which further deepens the association. Interrupting that loop means noticing the sensation without immediately catastrophizing about what it means. Instead of bracing, patients can loosen their grip and get curious. That kind of curious, non-threatening attention sends the nervous system a different message.

Over time, with consistent practice, the brain can learn that cold weather is just cold weather. The association weakens. The anticipatory firing quiets. This is not about positive thinking but about repeatedly giving the brain accurate information until it learns something new.

What This Means for Clinicians

Weather sensitivity is worth asking about directly, because patients often do not bring it up, either because they assume it is structural and therefore outside the scope of a mind-body conversation, or because they worry it will not be taken seriously.

A few questions worth incorporating:

Does your pain follow a seasonal pattern? What does winter feel like compared to summer? Do you notice your symptoms changing before the weather shifts, or only after? Can you think of a time when you expected weather-related pain and it did not show up? What was different?

That last question is particularly useful. Almost every patient with weather sensitivity can identify exceptions, times when the storm came and they were fine, times when they felt great in the cold. Those exceptions are clinical gold. They are evidence the cause is not structural, and they give you something to build on.

It is also worth gently exploring the seasonal affect dimension. Low mood, low energy, and increased pain sensitivity in winter are not separate problems. They are expressions of the same underlying shift in nervous system tone. Framing it that way for patients can reduce the sense of helplessness that winter often brings.

Actions to Take After Reading This Newsletter

1. If you notice weather-related pain, try observing it as a curious scientist would rather than as a worried patient. Where exactly is it? Does it shift? Is it as bad as you expected, or are you anticipating more than you are actually feeling?

2. Think back on the exceptions, times when the weather changed and your pain did not follow. They exist. What was happening those days?

3. If your symptoms worsen in winter, consider whether light exposure might be part of the picture. Morning light, in particular, is one of the most accessible and well-supported regulators of the nervous system.

4. If you are a clinician, add a weather-and-season question to your intake. The answers often reveal how much of the pain pattern is conditioned anticipation rather than structural change.

5. Notice if you have a story running about what winter means for your body. Beliefs about what the cold does to us can become self-fulfilling. The story is worth examining.

6. Share this newsletter with someone who tracks the weather through their pain. Understanding that the nervous system learned this pattern and can learn something else is often the most hopeful thing they will hear.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

This pattern is so common that patients and clinicians alike have come to accept it as part of living with chronic pain. But it doesn't have to be. There is a real explanation for why it happens, and understanding it changes what you can do about it.

The Distraction Factor

During the day, the brain is busy. Whether it’s work, conversations, screens, tasks, movement, or noise, the brain has something to process besides the body’s internal signals. This is not just a matter of taking your mind off things. It is a genuine neurological phenomenon.

The brain has a limited processing capacity, and attention is a resource that gets allocated. When external demands are high, the brain’s attention is directed outward, and pain doesn’t always win.

At night, that competition disappears. The room gets quiet. The phone goes down (hopefully). The to-do list pauses. And the brain, no longer occupied with the outside world, turns its attention inward toward the body, sensations, and anything that might register as a threat. For a nervous system that has learned to scan for danger, nighttime is when that scan runs at full volume.

This is why pain that felt manageable at two in the afternoon can feel unbearable at two in the morning. Nothing structurally changed — the brain’s attention did. Fewer competing inputs and distractions do not mean the sensation itself increased, but your attention and awareness of it may have.

The Circadian Rhythm Connection

There is also a biological piece to this that goes beyond attention. The body runs on a roughly 24-hour clock, the circadian rhythm, that regulates not just sleep and wakefulness but also hormones, immune activity, inflammation, and pain sensitivity.

Research has shown that several factors that modulate pain operate on a circadian schedule. Cortisol, which has anti-inflammatory effects, peaks in the morning and drops significantly in the evening and overnight. This means the body’s natural inflammation-buffering system is at its lowest exactly when most people are trying to sleep.

For people with neuroplastic pain including fibromyalgia, CRPS, and arthritis, this circadian fluctuation in the pain modulatory system is clinically meaningful. It is not that the underlying condition is getting worse at night. It is that the biological environment in which the pain is being processed shifts in a direction that makes symptoms more prominent.

The implication for treatment is important: addressing nighttime pain is not just about sleep hygiene. It is about understanding why the pain system is more active at those hours.

Quiet as a Threat Signal

Here is something that surprises many people: for a nervous system that has learned to associate stillness with danger, nighttime quiet is not calming. It is activating.

We covered this in an earlier newsletter about stillness and the brain’s tendency to fill quiet space with threat signals. But it is worth revisiting in the specific context of nighttime pain, because it is one of the most important and least understood pieces of this picture.

During the day, the body is moving. Movement provides proprioceptive feedback, information about where the body is in space, how the muscles and joints are loaded, and what is happening at the physical level. That feedback can be reassuring to the nervous system. It is data about the body that does not read as threat.

When you lie still in the dark, you have less of that proprioceptive feedback. The body is no longer moving, no longer providing the same stream of neutral signals.

Think of it like a guard dog that barks not because it heard something, but because it suddenly stopped hearing anything. The nervous system interprets that absence of data as suspicious and starts generating its own signals to fill the gap. For some people, this shows up as hyperawareness of heartbeat or breathing. For others, it shows up as pain.

This is particularly relevant for people whose pain began around a time of high fear or helplessness: an illness, an injury, a period of significant life stress or loss. Someone who spent nights lying awake in pain, waiting to see if it would get worse, may have inadvertently taught their nervous system that lying still in the dark means danger is coming. Bedtime becomes a conditioned cue, and the brain fires its protective signals on schedule.

The Preoccupation Loop

There is one more piece worth naming: nighttime removes not just distraction but also the social scaffolding of the day. There are no colleagues to talk to, no tasks demanding your focus, no external reality to anchor you. It is just you and your thoughts.

For people with chronic pain, those nighttime thoughts often run in a predictable direction: scanning the body, interpreting sensations, catastrophizing about what tomorrow will feel like, replaying the day’s symptoms, anticipating the next flare. This is the preoccupation loop. It is one of the most reliable ways to amplify pain, and it can become strangely hard to let go of. When the alternative is lying in the dark with nothing to focus on, the loop, however exhausting, starts to feel familiar. It can even feel somewhat productive, like you are staying on top of something, preparing, managing. That familiar response begins to feel safe — like home. And so the brain returns to it, night after night.

What makes this especially powerful is that the brain does not readily distinguish between a threat that is happening now and one that is vividly imagined. Catastrophic thinking about pain activates the same threat-response pathways as pain itself. At night, lying still in the dark with nothing else to focus on, that loop can run unchecked for hours.

Understanding this loop is not about telling patients to think more positively. It is about helping them recognize what is actually driving the escalation. Noticing when the loop has started is often the first interruption to breaking it.

The science on why nighttime pain is worse has been building for over a decade, and three findings in particular are worth holding onto. A landmark review by Finan, Goodin, and Smith published in The Journal of Pain found that sleep disturbance predicts next-day pain more strongly than pain predicts next-day sleep. In other words, poor sleep is not just a symptom of chronic pain. It is one of its most reliable drivers. Addressing sleep is not a secondary concern in pain recovery, but a primary one.

The circadian dimension of nighttime pain has also been increasingly well-documented. The cortisol and cytokine shifts described earlier in this newsletter are not unique to any one condition. Research published in Acta Physiologica confirmed that both headache and neuropathic pain follow the same predictable daily patterns, tied to the same internal clock. What this means practically is that the body’s vulnerability window at night is not random, it is scheduled.

A 2024 narrative review in Clinics and Practice synthesizing research across multiple chronic pain conditions confirmed that sleep impairment is a central feature across low back pain, orofacial pain, joint pain, headaches, and fibromyalgia, and that the relationship runs in both directions, with each condition capable of worsening the other over time. The takeaway is not that chronic pain and sleep problems are hopelessly entangled. It is that addressing one is one of the most direct routes to improving the other.

Finan PH, Goodin BR, Smith MT. The association of sleep and pain: an update and a path forward. J Pain. 2013;14(12):1539–1552.

Burish MJ, Chen Z, Yoo SH. Emerging relevance of circadian rhythms in headaches and neuropathic pain. Acta Physiologica. 2019;225(1):e13161.

Jain SV, Panjeton GD, Martins YC. Relationship between sleep disturbances and chronic pain: a narrative review. Clinics and Practice. 2024;14(6):2650–2660.

The Insomnia Connection

We covered insomnia in a previous newsletter, and it is worth briefly naming the connection here. Sleep deprivation and chronic pain have a deeply bidirectional relationship. Poor sleep amplifies pain, and pain disrupts sleep, creating a cycle that can become self-sustaining.

Research consistently shows that even one night of poor sleep can lower pain thresholds significantly the following day. A sensation that would normally read as neutral can suddenly trigger a response that feels completely out of proportion. Over time, chronic sleep disruption changes how the nervous system processes pain at a functional level. This is not just fatigue making everything feel worse. It is the pain modulatory system being functionally compromised by insufficient rest.

This means that addressing nighttime pain is not just about comfort. It is one of the most high-leverage interventions available in chronic pain care. When the sleep-pain cycle starts to shift, patients often report that daytime symptoms shift too. Not because anything changed during the day, but because the nervous system finally got the recovery time it needed. Sleep is not separate from pain recovery. For many people, it is where recovery actually happens.

What This Means for PRT

The four mechanisms described in this newsletter — reduced distraction, circadian vulnerability, quiet as a threat signal, and the preoccupation loop — are not separate problems requiring separate solutions. They are all expressions of a nervous system that has learned to treat certain conditions as dangerous. And a nervous system that has learned something can learn something else.

PRT is particularly well-suited to nighttime pain because it works directly with the threat-appraisal process. When a patient practices approaching nighttime sensations with curiosity rather than bracing against them, noticing where the sensation is, what it actually feels like, and whether it shifts with attention, they are doing something specific at the neurological level. They are sending the brain a safety signal at the exact moment the brain is scanning hardest for danger. Over time, that changes the association. Bedtime stops being a conditioned cue for escalation and starts to become something more neutral.

The preoccupation loop is also directly addressable in PRT. A core part of the work is helping patients recognize the difference between a sensation and their story about what that sensation means. Noticing tightness in the lower back is not the same as catastrophizing about what tomorrow will feel like. That distinction is harder to hold at two in the morning than at two in the afternoon, which is exactly why practicing it during the day matters. The nervous system is more available for learning when it is less activated, and that learning transfers.

For patients whose nighttime pain is tied to a period of fear or helplessness, an illness, an injury, a time when lying still genuinely was associated with something frightening, the work also involves gently updating that association. The body is safe now. Stillness is safe now. The nervous system learned the opposite, and it can learn again.

Huberman Lab Podcast: “Master Your Sleep and Be More Alert When Awake” Andrew Huberman

This one is a listen, not a read, but it belongs here. If the biology in this newsletter resonated with you, this episode is a natural next step. Huberman breaks down the science of sleep and wakefulness, covering circadian rhythms, the role of cortisol and light in regulating your internal clock, and what actually happens in the brain and body when sleep goes wrong. Accessible, detailed, and free.

🎧 Master Your Sleep and Be More Alert When Awake

Actions to Take After Reading This Newsletter

1. If your pain is consistently worse at night, consider whether the distraction factor, circadian shifts, or the preoccupation loop might be contributing, and which feels most relevant to your experience.

2. Notice what you are thinking about when your pain builds at night. Are you scanning for danger, catastrophizing, or anticipating tomorrow? Naming the pattern is the first step to interrupting it.

3. Try approaching nighttime sensations with curiosity rather than urgency. Instead of trying to make the pain stop, get interested in it. Where exactly is it? What does it feel like? Does it shift when you breathe or simply when you watch it?

4. If you are a clinician, add a nighttime pain question to your standard assessment. When does it start? What is the patient doing and thinking when it peaks? The answers often reveal the conditioning patterns driving the cycle.

5. If sleep has felt like a lost cause, consider reframing it as one of the most direct interventions available for pain recovery. Treating it as a priority, not an afterthought, changes what you do with your evenings.

6. Share this newsletter with someone who has been told that nighttime pain flares are just part of their condition. Understanding why it happens is often the beginning of it changing.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

You worry constantly, and somewhere underneath all of that worry, if you’re honest, there might be frustration too, and then guilt for feeling frustrated.

That part is not talked about enough.

This week’s newsletter is for the people in the room who aren’t the patient. The spouses, the parents, the adult children, the siblings and close friends who are showing up every day for someone in pain and carrying their own invisible weight while doing it. And it’s also for the clinicians who treat those patients, because what’s happening in the caregiver relationship is almost always part of what’s happening in the pain.

The Caregiver Is Not Just a Bystander

When someone lives with chronic pain, the people closest to them are also deeply affected. Research consistently shows that family members and partners of people with chronic pain experience elevated levels of stress, anxiety, and psychological distress, and that over time, without support, caregivers can develop their own health consequences from the sustained strain of the role.

But the relationship between caregiver and patient isn’t just about the caregiver’s wellbeing in isolation. It’s bidirectional in ways that matter deeply for the person in pain.

A 2023 study published in Frontiers in Behavioral Neuroscience found that a caregiver’s pain-related beliefs directly influence a patient’s coping strategies, mediated through emotion regulation. In other words, how a caregiver thinks about and responds to pain shapes how the patient relates to their own pain. If a caregiver believes movement is dangerous, the patient is more likely to avoid movement. If a caregiver responds to pain expressions with alarm, the patient’s nervous system registers that alarm as confirmation of threat. If a caregiver is calm, curious, and encouraging, the environment around the pain changes, and so does the pain.

This is not blame. It is biology. And it is one of the most important and underappreciated levers in chronic pain recovery.

Alinajimi, F., Deldar, Z., Dehghani, M., & Khatibi, A. (2023). Emotion regulation mediates the relationship between family caregivers’ pain-related beliefs and patients’ coping strategies. Frontiers in Behavioral Neuroscience, 17. https://doi.org/10.3389/fnbeh.2023.983350

What Helps and What Doesn’t

Most caregivers err on one of two sides, both born of love and both of which can inadvertently make things harder.

The first is overprotection. Doing things for the person in pain that they could do themselves, steering them away from activities out of fear, treating them as fragile.

This pattern, however loving, sends a clear message to the nervous system: you are not safe, your body cannot be trusted, you need to be protected from yourself. For someone trying to learn that their body is safe, that message runs directly counter to the goal.

The second is the opposite: minimizing or dismissing. Telling someone to push through, expressing frustration at the limitations the pain creates, implying that things should be better by now. This pattern, however understandable given the exhaustion of the caregiver role, creates a different problem: the person in pain stops feeling safe enough to be honest about where they are, and isolation grows on top of everything else.

What actually helps sits in a different place entirely. It is the caregiver who can say: I believe you, and I also believe you can get through this. Who can be present without being consumed. Who can learn enough about the science of pain to understand why their own responses matter, not to put pressure on themselves, but to become a genuine part of the healing environment.

That is a skill. It can be learned. And it makes a real difference.

The Caregiver Approach

When someone you love — a parent, child, partner, sibling, or close friend — has chronic pain or other chronic symptoms, it hurts to see them struggling. You may go to great lengths to help them — search for alternative treatments, set them up with specialists, have tests run and rerun, wait on them after surgery — only for them to experience little to no relief. Or maybe something sparks hope, helping briefly, only for them to end up back where they started. Your approach to caregiving may be instinctive, selfless, and overwhelmingly positive, but once your loved one starts Pain Reprocessing Therapy, your approach may actually need to shift.

Caregivers need support just as much as patients do. Caregiving is hard, exhausting work, and taking care of yourself is pivotal. Turns out, it can actually be supportive for your loved one to enjoy life again, and you can be that model for them.

And remember, you are not alone. There are over 50 million people in the US alone suffering from chronic pain, and millions of caregivers!

There is a dynamic that shows up frequently in chronic pain families that rarely gets named out loud: the way that pain, over time, can quietly restructure an entire relationship.

Roles shift. The person in pain may become the one who is cared for in ways that change how both people see themselves in the relationship. Plans get made around the pain. Social life contracts. The caregiver’s needs can start to feel illegitimate by comparison; after all, they’re not the one suffering. So those needs go unvoiced, and resentment quietly builds beneath the surface of genuine love and care.

Research published in a 2025 review on the impact of chronic pain on families found that families highly impacted by pain can be marked by emotional dysregulation, role tension, cycles of invalidation, and the suppression of anger, frustration, and despair on both sides. Family members may blame themselves for being unable to soothe their loved one’s pain. And people living with chronic pain often report significant unmet needs for emotional validation alongside feeling that they are being misunderstood or disbelieved, sometimes even by the people closest to them.

Both people in these dynamics are suffering. Both deserve support. And the conversation between them, what it sounds like, what it makes possible or forecloses, has real consequences for recovery.

De La Rosa, J. S., Herder, K. E., Romero, R. D., Wolf, D. S., Largent-Milnes, T., Ibrahim, M. M., et al. (2025). Impact of chronic pain on the families of U.S. adults. medRxiv. https://doi.org/10.1101/2025.02.28.25322828

What This Means for Clinicians

For practitioners working with chronic pain patients, the caregiver relationship is clinical territory worth exploring.

When a patient’s progress stalls, when fear keeps reasserting itself, or when the home environment seems to be working against the gains made in session, asking about the relational context is often where the most important information lives. Not to assign blame to a partner or family member, but to understand the full system the nervous system is living in.

Some questions worth bringing into the room:

How do the people around you respond when your pain increases? Do you feel believed? Do you feel pressure to seem better than you are? Is there space in your relationship to talk about this honestly? What do your loved ones think of your diagnosis, or lack of one?

And for caregivers who are present in treatment or who come in on their own: What do you need? How are you coping? What are you carrying that hasn’t been named yet? What would it mean to you if your loved one got better?

That last question sometimes surprises people, but it is worth asking. Pain changes relationships, and so does recovery. And for some caregivers, that change feels unconsciously uncertain in ways worth understanding.

You Don’t Have to Figure This Out Alone

If you are a caregiver looking for real answers about what your loved one is going through, what actually helps, and what the road to recovery looks like, we want to give you a space to ask.

On Thursday, June 11, WellBody therapists Danielle Adams O’Malley, LCSW, and Hans Sieber, LPC, are hosting a free, live 60-minute Q&A designed specifically for caregivers and family members of people with pain and other chronic symptoms, including but not limited to dizziness and vestibular disorders, fatigue, IBS, insomnia, and more.

This is not a lecture. It is a conversation built around your questions, your specific situation, and the things you have been carrying without enough support.

The webinar will cover:

• What chronic pain is, what causes it, and why it’s not “all in their head”

• What your loved one is learning through the process of Pain Reprocessing Therapy

• Natural and well-meaning caregiver pitfalls with more supportive alternatives

• What helps and what doesn’t when supporting someone through chronic pain, especially a PRT patient

• Habits that lead to caregiver exhaustion (and usually don’t help the patient)

• Why your own self-care will actually help support the person you are worried about

• Answers to your specific questions, submitted at registration

When Someone You Love Is in Pain: A Live Q&A for Caregivers 📅 Thursday, June 11 | 1–2 PM EST | Free

Register here

Can’t make the live webinar? Register anyway to submit your questions and receive a recording of the session!

A note from our facilitator, Danielle Adams O’Malley:

Watching my daughter lose 10 years of her childhood to chronic MdDS was the most painful and isolating experience of my adult life. My emotions were spilling everywhere with no place to go. I grew tired of explaining her inexplicable condition to family and friends over and over again, only to feel misunderstood and further alone.

The fallout of a chronic condition for a child — academic, social, developmental, and psychological — is profound. And for the parent, who by default becomes the caregiver, the fear and helplessness are unbounded. The prescriptions were endless, the tests were benign, and the therapies did nothing and at times, worsened her symptoms.

It wasn’t until discovering PRT that my daughter truly felt relief. She still has flare-ups. But PRT has given her a cognitive and emotional understanding of her symptoms and tools to neutralize the fear that no doctor or prescription could ever treat.

Because of PRT, we can now trust that the worst is in the rearview mirror. My daughter is good and thriving. But that vehicle I drove through that 10-year storm still has some dents. As a mom and caregiver, I’ve often thought the journey could have been much less hazardous if I only had a community of parents and other caregivers who understood the pain, confusion, and worry of being a caregiver of a loved one with chronic illness.

Now, as a therapist specializing in chronic pain/conditions and trauma, I am grateful to lend my personal and professional experience to help make the caregiving journey much less isolating.

The Pain Reprocessing Therapy Workbook for Teens

Daniella Deutsch, LCSW | Penina Zilberberg, PhD | Paulina Soble, LCSW

Written for teens, but built just as much for the adults around them — parents, teachers, coaches, and clinicians. If you are supporting a young person with chronic pain and have felt like you didn’t have the right language or tools to help, this workbook was made with you in mind, too.

Inside, teens learn to break the chronic pain loop with repeatable, brain-based skills, read their body signs more accurately, and reconnect brain and body so that safety becomes the default. Step-by-step practices like breathwork, cognitive reappraisal, pacing, and gentle exposure are paired with ready-to-go scripts, worksheets, and progress trackers, so the work doesn’t stay in session. It comes home.

Children believe they are as capable as their parents make them feel. This workbook gives everyone in the room the same language, the same framework, and the same confidence to move forward together.

Get the workbook

Actions to Take After Reading This Newsletter

1. If you are a caregiver, notice this week whether your responses to your loved one’s pain tend toward overprotection, minimizing, or something else — without judgment, just with curiosity.

2. Consider whether your own needs are being named and met in the relationship, or whether they’ve quietly been set aside.

3. If you are a patient, consider what your loved one might need to better understand your experience — and whether there is a conversation worth having.

4. If you are a clinician, consider asking about the caregiver relationship in your next session with a patient whose progress feels stuck. The answer may open a door.

5. Register for the June 11th caregiver Q&A, and share it with someone in your life who is supporting a person in pain. This one is for them.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

That is changing. Not because stress is being taken less seriously, but because the science of how stress actually produces physical symptoms has become specific enough, and well-documented enough, that it can no longer be waved away as vague or purely psychological.

This week, we want to walk through what that science shows, because understanding the mechanism behind stress and physical symptoms is not only interesting, but for people in pain, it can be one of the most clarifying things to learn.

The Body Is Always Listening to the Brain

The starting point for understanding how stress causes physical symptoms is the same place we return to again and again: the autonomic nervous system.

The ANS is the part of the brain that runs the body on autopilot, regulating heart rate, digestion, immune response, skin, and hundreds of other functions without any conscious input from us. It is also the part of the brain that responds to perceived threat by activating the stress response: releasing cortisol and adrenaline, tensing muscles, redirecting blood flow, and putting the immune system on high alert.

This system was designed for short-term emergencies. Activate, respond, recover.

The problem is that the modern nervous system is frequently activated without ever fully recovering — and when the stress response runs continuously, its downstream effects on the body become cumulative, measurable, and sometimes severe.

What researchers have increasingly been able to do is trace those downstream effects with enough specificity to identify exactly which neurons are involved, which immune pathways they activate, and what the physical result looks like. The picture that emerges is not vague. It is a precise biological chain of events.

Eczema: A New Window Into the Stress-Body Connection

A recent study published in Science offered a clear demonstration of how stress translates into physical inflammation, this time in the skin.

The research focused on atopic dermatitis, a form of chronic eczema affecting more than 200 million people worldwide. It has long been observed that stress makes eczema worse. What hasn’t been clear is exactly how, or what biological pathway connects a psychological state to inflamed skin.

The researchers identified a specific network of neurons in the skin that respond to stress signals from the central nervous system. When psychological stress was experienced, these neurons activated immune cells called eosinophils, driving them into the skin tissue and fueling inflammation. In a mouse model of the condition, stressed animals had four times as many eosinophils in their skin as non-stressed controls! Activating these stress-responsive neurons more than doubled the accumulation of immune cells. And blocking them stopped stress from worsening symptoms entirely.

As co-author Shenbin Liu, neurobiologist at Fudan University, put it, this study shows how a feeling — psychological stress — can translate into a biological event, namely inflamed skin.

This is a measurable, traceable, neuron-by-neuron pathway from the emotional state to the physical symptom. And what is true for eczema is increasingly being shown to hold true across a wide range of conditions.

Naddaf M. How stress causes an eczema flare-up. Scientific American. March 22, 2026.

CRPS: When the Brain Becomes the Pain Generator

Complex Regional Pain Syndrome, CRPS, is one of the most striking examples of what happens when the nervous system’s sensitization process goes into overdrive.

CRPS typically begins after an injury, sometimes a minor one. It most commonly affects one limb, usually an arm, leg, hand, or foot. What follows is a pain response that is out of proportion to any ongoing tissue damage, and that, in many cases, persists long after the original injury has healed. The affected limb may become hypersensitive to touch, temperature, and movement. The pain can spread. The impacted limb will often show noticeable differences in skin temperature, color, and texture. And in one of the more remarkable findings in pain neuroscience, research from the IASP has shown that people with CRPS experience increased pain simply from thinking about moving the affected body part, without moving it at all.

In another study, when patients watched a mirror reflection of their unaffected limb being touched, tricking the brain into perceiving that the painful limb was being touched, they experienced pain as if it had actually been touched. The brain, not the tissue, was generating the pain signal.

This is what central sensitization looks like at its most visible. The nervous system has become so broadly amplified, so primed for threat, that the normal thresholds for pain no longer apply. What would be a neutral sensation for most people registers as agony. What would be a simple thought registers as a physical event.

CRPS is an extreme case, but it illustrates a principle that applies across the spectrum of chronic pain conditions: the nervous system can become a primary driver of symptoms, independent of ongoing tissue damage. And stress, the sustained activation of the threat response, is one of the most reliable ways that sensitization develops and deepens over time.

Moseley, G. L. (2008). The effect of motor imagery on pain and swelling in people with complex regional pain syndrome. Current Rheumatology Reviews, 4(1), 1–5.

McCabe, C. S., Haigh, R. C., Halligan, P. W., & Blake, D. R. (2003). Referred sensations in patients with complex regional pain syndrome type 1. Rheumatology, 42(9), 1067–1073.

The Immune System and the Nervous System

One of the most important shifts in pain science over the past decade is the recognition that the nervous system and the immune system are not separate entities that occasionally interact. They are deeply integrated, communicating constantly through overlapping chemical signals, each capable of amplifying the other’s responses.

When the stress response activates, it does not only affect muscles and heart rate. It directly modulates immune function, sometimes suppressing it in the short term, and in conditions of chronic stress, dysregulating it in ways that contribute to inflammation, heightened pain sensitivity, and a range of physical symptoms that look, from the outside, like purely physical disease.

This is the mechanism behind why people with histories of chronic stress or trauma are more vulnerable to conditions like fibromyalgia, irritable bowel syndrome, psoriasis, and more. Diagnoses like Crohn’s and Ulcerative Colitis are real inflammatory autoimmune-related diseases that involve measurable inflammation in the digestive tract and require medical attention. That said, the nervous system and stress can strongly influence flare severity, pain intensity, and frequency.

Substantial research shows that chronic stress, trauma, anxiety, and nervous system dysregulation can affect the gut-immune axis. Patients with symptoms of gut inflammation may notice pain worsen during times of high stress, emotional conflict, burnout, sleep deprivation, or other major life changes.

The inflammation is real. But the nervous system can influence how intensely it is experienced and expressed.

For patients who have been told that their symptoms are stress-related and felt dismissed, this science offers something different: not a dismissal, but an explanation. The stress is not replacing the physical symptom. It is producing or amplifying it through a real biological pathway that can be identified, understood, and in many cases, addressed.

Moseley GL. The brain in CRPS — more barriers or new opportunities? IASP Relief News. iasp-pain.org.

Ge, L., et al. (2022). Psychological stress in inflammatory bowel disease. Frontiers in Psychiatry, 13, 1018249.

Bonaz, B., Sinniger, V., & Pellissier, S. (2024). Role of stress and early-life stress in the pathogeny of inflammatory bowel disease. Frontiers in Neuroscience, 18, 1458918.

Inflammation and Pain

There is actually a distinction between pain driven by active tissue inflammation and pain driven by altered nervous system processing. Pain does not correlate perfectly with inflammation, as the brain and nervous system can amplify, sustain, or generate pain even when inflammation is unchanged or absent. In a study on long COVID patients, researchers originally believed chronic symptoms were being caused by ongoing inflammation from inflammatory cytokines. But what was found among those who recovered was no significant changes in cytokines. Instead, the applied treatment regulated the autonomic nervous system, and symptom improvement happened without measurable change in inflammatory markers.

Verbanck, P., Clarinval, A. M., Burton, F., Corazza, F., Nagant, C., & Cheron, G. (2021). Transcutaneous Auricular Vagus Nerve Stimulation (tVNS) can Reverse the Manifestations of the Long-COVID Syndrome: A Pilot Study. Advances in Neurology and Neuroscience Research, 2, Article 100011.

What This Means for PRT

Pain Reprocessing Therapy operates in exactly this territory.

When PRT helps a patient reduce fear around their symptom, practice approaching sensations with curiosity rather than alarm, and gradually reappraise what their nervous system is signaling — what is happening biologically is that the threat response is being downregulated. The stress signal to the immune system, the skin, the gut, the muscles, is being quieted. The sensitization that has built up through repeated activation is being given the conditions it needs to resolve.

This is why the question “can stress really cause physical symptoms?” is not just academically interesting. For anyone working in this space, as a patient or a clinician, the answer shapes how treatment is understood, how recovery is framed, and how much hope is reasonable to hold.

The answer, supported by a growing and increasingly precise body of evidence, is yes. Stress causes physical symptoms through real, traceable, biological pathways.

And those pathways can change.

Ready to Work With Someone Who Understands?

If you have been living with symptoms that stress makes worse, that don’t show up cleanly on tests, or that haven’t responded to treatments that should have worked, you are not imagining it. And you don’t have to keep searching for answers alone.

WellBody Psychotherapy specializes in exactly this. Our therapists are trained in Pain Reprocessing Therapy and understand the science behind how stress, the nervous system, and physical symptoms are connected. We work with adults and adolescents, and we are here when you are ready.

Schedule an intake here

Actions to Take After Reading This Newsletter

1. If you have been told your symptoms are stress-related and felt dismissed, consider whether this newsletter reframes that explanation in a way that feels more useful and more accurate.

2. Notice this week whether your symptoms fluctuate with your stress levels, better during calm periods, worse during difficult ones. That pattern is clinically meaningful data, not a coincidence.

3. If you are a clinician, consider how you explain the stress-symptom connection to patients who are skeptical or who have felt dismissed by that framing. Having specific, mechanistic language, neurons, immune cells, and sensitization can make the conversation land very differently.

4. Think about what the eczema study means more broadly: if stress can activate specific neurons that drive immune cells into the skin, the same principle of nervous system to body communication applies to pain, fatigue, gut symptoms, and more.

5. Share this newsletter with someone who is still looking for a biological explanation for their symptoms. The science is here. It just hasn’t reached everyone yet.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com

But let’s first focus on the postpartum physical symptoms that are not just present in the weeks right after birth, but for months and sometimes years. These symptoms so often get lumped into a few familiar categories: baby blues, postpartum depression, and postpartum anxiety. Those are real and they matter. But there is a whole layer of the postpartum experience that rarely gets named clearly — these physical symptoms that don’t fit neatly into a psychiatric diagnosis, but don’t go away on their own either. Persistent pain. Fatigue that sleep doesn’t fix. Headaches, dizziness, gut symptoms, hypersensitivity to sound and light and touch. A body that feels fundamentally different and not in a way anyone warned you about.

For many people, what’s happening in those moments is not purely structural, not a sign of lasting physical damage, and not something that just needs more time. In fact, the nervous system is actually doing what a nervous system does when it has been through something enormous and is still trying to figure out if the threat is over. And we say that not to minimize the experience, but because we think it deserves an accurate explanation.

A note on where this one comes from: both of the people behind this newsletter became mothers to new babies this year, with one of us actually just returning from maternity leave this week. We did not choose this topic from a research list. We chose it because we have been living it and because the framework we spend our weeks writing about has been enormously relevant and helpful in our own experiences.

The Postpartum Nervous System Is Not the Same Nervous System

Pregnancy and childbirth put the nervous system through one of the most significant experiences of a lifetime. From a biomedical perspective, everything shifts hormonally, neurologically, and physiologically. And while much of that is normal and expected, it also means that the nervous system arrives at the postpartum period in a heightened, sensitized state.

This matters because a sensitized nervous system is more likely to interpret neutral signals as threatening. It is more likely to produce pain, fatigue, and other symptoms in response to inputs that would not have triggered them before. And it is more likely to stay in a state of chronic low-grade activation, that constant hum of alert that never fully settles.

For new parents, those reasons are not hard to find. Sleep deprivation alone is a significant nervous system stressor. Add in the responsibility of keeping a new human alive, the recovery from a physically demanding birth, the significant hormonal crash that follows, the shift in identity and relationships, and the relentless unpredictability of early parenthood, and you have a nervous system that is being asked to recalibrate in conditions that are not exactly conducive to calm.

A 2024 review of persistent postpartum pain described the combination of biological and psychological factors at play in this period as a somatic and psychologic perfect storm. That framing is apt and so incredibly validating to us moms. The symptoms are real, and the conditions that produce them involve so many overlapping systems at once.

Horvath B, Kloesel B, Cross SN. Persistent postpartum pain: a somatic and psychologic perfect storm. J Pain Res. 2024;17:35-44.

The Fear-Pain Connection Is Especially Active Postpartum

Fear is a normal and adaptive part of early parenthood. The nervous system is designed to be more alert when a vulnerable new life depends on you. In evolutionary terms, a new parent’s heightened threat detection makes sense.

But when that threat detection system stays chronically activated, when every sound becomes a potential danger, when the body is always bracing, when intrusive thoughts about potential harm to the baby keep the amygdala firing even in quiet moments, the nervous system can begin generating physical symptoms as a consequence of that sustained fear.

Research consistently shows that anxiety and fear sensitize the pain system, lowering the threshold at which signals are interpreted as threatening and amplifying the intensity of symptoms. Postpartum anxiety affects up to 20% of new mothers and is frequently underdiagnosed, in part because many of its physical expressions, including body tension, headaches, gastrointestinal symptoms, and fatigue, are attributed to the demands of new parenthood rather than recognized as symptoms that deserve attention.

If you look at this through the lens of the fear-avoidance model, fear of pain leads to avoidance, which leads to further sensitization and reduced function. In the postpartum context, this loop can form quickly: a new parent who is already hypervigilant experiences physical symptoms, interprets them as danger signs, avoids the movements that trigger them, becomes more anxious, and watches the symptoms intensify in response.

Interrupting that loop early with psychoeducation, normalization, and accurate information about what is driving the symptoms is one of the most powerful things a clinician can do.

Fairbrother N, Janssen P, Antony MM, Tucker E, Young AH. Perinatal anxiety disorder prevalence and incidence. J Affect Disord. 2016;200:148–155.

Vlaeyen JWS, Linton SJ. Fear-avoidance and its consequences in chronic musculoskeletal pain: a state of the art. Pain. 2000;85(3):317–332.

PRT with Postpartum Patients

Pain Reprocessing Therapy works by helping the brain learn that the body is safe. In the postpartum period, communicating authentic safety requires an additional layer of acknowledgment: the nervous system did not become sensitized for no reason. It was doing exactly what it was built to do.

When a PRT therapist works with a postpartum patient, the goal is not to talk them out of their symptoms or to convince them that birth was fine. It is to help the nervous system complete the recalibration that got interrupted by months of sleep deprivation, sustained vigilance, and the physical and emotional enormity of what they went through. Safety messages are not platitudes. In this context, they are a direct intervention on a threat-detection system that has been running on high consistently over a long period of time.

There is also something particularly meaningful about PRT with postpartum patients around identity, and it is worth slowing down here, because this layer of the postpartum experience is one that rarely gets the clinical attention it deserves.

Chronic pain, on its own, is already a destabilizing force when it comes to sense of self. People in persistent pain may lose not just function, but identity. They lose the version of themselves who could do the things they used to do, who showed up in relationships the way they used to, and who felt at home in their own body. They grieve a self that isn’t entirely gone but isn’t quite accessible either. In our clinic, WellBody Psychotherapy, we see this constantly: the person who says “I don’t know who I am anymore” is not being dramatic. They are describing something real about what chronic pain does to one’s sense of continuity and self.

Becoming a mother adds an entirely separate layer of that same experience, regardless of how wanted or celebrated the baby is. It involves a profound reorganization of identity that our culture dramatically underprepares people for. You are not the same person you were before. Your relationships shift. Your sense of your own body shifts. Your sense of what you want, what you need, and who you are outside of this new role is suddenly in question. Anthropologist Dana Raphael, who coined the term matrescence in the 1970s, described it as a developmental passage as significant as adolescence. And like adolescence, it is disorienting by nature.

When postpartum pain enters that picture, the two experiences compound each other in ways that can be genuinely overwhelming. A person is already working to figure out who they are now that they are a mother, and their body is simultaneously producing symptoms that make them feel even less like themselves. The nervous system does not treat identity uncertainty as a philosophical question — it treats it as a threat signal. Not knowing who you are, not recognizing your own body, and not being able to predict how you will feel from one hour to the next registers as danger to the brain. And a nervous system that detects danger produces more symptoms. The symptom-fear feedback loop strengthens.

PRT’s emphasis on curiosity over fear, on approaching symptoms with interest rather than alarm, offers a foothold in a period where so much feels out of control. But perhaps more importantly, PRT holds a fundamentally compassionate view of the person in pain — not as someone who is broken, weak, or failing at recovery, but as someone whose nervous system is responding logically to an enormous amount of input. That reframe matters especially here. The postpartum person who is struggling with pain and identity loss does not need to be told to think more positively. They need to be told that what is happening to them makes sense, and that their nervous system can learn something new, making recovery possible.

What This Means for Clinicians

The postpartum period is one where early recognition can make a significant difference. A few things worth considering when working with postpartum patients:

Persistent physical symptoms deserve a thorough assessment. Normal postpartum recovery has a general timeline. Symptoms that persist well beyond it, or that never tracked clearly with physical findings, warrant a broader lens.

Ask about the emotional and relational context, not just the physical one. How was the birth experience? Was there fear or trauma involved? What does anxiety look like day to day? How is sleep? What are the relationships like? Have those relationships shifted? The answers often tell you more than the symptom description alone.

Normalize the nervous system explanation early. Many postpartum patients have been told their symptoms are “just stress” or “just part of having a baby” and they resent it, because it doesn’t feel like an explanation — it feels like a dismissal. Reframing through the lens of central sensitization and nervous system recalibration gives them something real to hold onto. It validates biology without implying permanent damage or being dismissive.

Screen for birth-related fear and trauma. Not every difficult birth meets criteria for PTSD, but fear and helplessness during childbirth are potent nervous system activators that often don’t surface in standard postpartum assessments. Ask directly. The window is narrow and the clinical return is high.

Assess for Dysphoric Milk Ejection Reflex (D-MER). This is a physiological condition where breastfeeding or pumping triggers a sudden, brief wave of negative emotions — sadness, dread, irritability, hopelessness, anxiety, nausea, or restlessness. If your patient is nursing, this may be something to assess for in order to provide an appropriate diagnosis and treatment course. D-MER is separate from postpartum anxiety or depression, though they often get grouped together.

Ready to Work With Someone Who Understands?

If you are in the postpartum period and experiencing symptoms that don’t seem to be resolving, that feel disconnected from what tests are showing, or that are being dismissed as a normal part of new parenthood — you deserve more than “give it time.”

WellBody Psychotherapy works with people navigating exactly these kinds of issues.

Schedule an intake here

Actions to Take After Reading This Newsletter

1. If you are in the postpartum period and experiencing persistent physical symptoms, consider whether the nervous system context described here resonates with your experience. You are not imagining it, and you are not alone.

2. Notice whether your symptoms fluctuate with your emotional state, your sleep, your anxiety level. That pattern is meaningful information, not a coincidence.

3. If you are a clinician, consider asking postpartum patients not just about their physical recovery but about their fear, their anxiety, and their emotional experience of early parenthood. The answers often open clinical doors that the physical history alone does not.

4. Share this newsletter with someone in the postpartum period who has been told their symptoms are just part of having a baby. Sometimes having the language and validation for what is happening is the first thing that helps.

5. If you are supporting a new parent who seems to be struggling beyond what early parenthood usually looks like, encourage them to seek support. The postpartum nervous system is treatable. They do not have to wait it out alone, and full recovery is possible.

For upcoming trainings, workshops, and events, visit painreprocessingtherapy.com