{"id":8061,"date":"2026-07-19T14:43:17","date_gmt":"2026-07-19T12:43:17","guid":{"rendered":"https:\/\/blueportance.com\/knowledge-base\/expert-guides\/understanding-pain\/neurosensory-deprogramming\/"},"modified":"2026-10-25T22:43:27","modified_gmt":"2026-10-25T21:43:27","slug":"neurosensory-deprogramming","status":"publish","type":"page","link":"https:\/\/blueportance.com\/en\/knowledge-base\/expert-guides\/understanding-pain\/neurosensory-deprogramming\/","title":{"rendered":"KB 3_Expert Guide_01_Understanding Pain_08_Neurosensory Deprogramming"},"content":{"rendered":"\n\n<style>\n    body{font-family:Arial,sans-serif;line-height:1.65;padding:20px;color:#333}\n    .bp-q-breadcrumb{font-size:.85rem;color:#6b7280;margin:0 0 20px}\n    .bp-q-breadcrumb a{color:#2a7fba;text-decoration:none}\n    h1{color:#0e2a47;font-size:1.8rem;line-height:1.25;margin:0 0 22px}\n    h2{color:#1a4d72;margin-top:42px;line-height:1.3}\n    h3{color:#0e2a47;margin-top:28px}\n    p{margin:0 0 16px}\n    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  .bp-bdc-toc{background:#f8fbff;border:1px solid #dbeaf7;border-radius:9px;padding:18px 22px;margin:24px 0 32px}\n    .bp-bdc-toc h2{margin:0 0 10px;font-size:1rem;color:#1a4d72}\n    .bp-bdc-toc ul{margin:0;padding-left:20px;list-style:none}\n    .bp-bdc-toc li{margin-bottom:6px;font-size:.92rem}\n    .bp-bdc-toc a{color:#2a7fba;text-decoration:none}\n    .bp-bdc-toc a:hover{text-decoration:underline}\n  <\/style>\n<style>\n.bp-bdc-breadcrumb{max-width:900px;margin:0 auto;padding:20px 16px 0;font-size:.85rem;color:#6b7280;}\n.bp-bdc-breadcrumb a{color:#2a7fba;text-decoration:none;}\n.bp-bdc-breadcrumb a:hover{text-decoration:underline;}\n<\/style>\n\n<nav class=\"bp-bdc-breadcrumb\" aria-label=\"Breadcrumb\">\n<a href=\"\/en\/\">Blue Portance<\/a> \u2192 <a href=\"https:\/\/blueportance.com\/en\/knowledge-base\/\">Knowledge Base<\/a> \u2192 <a href=\"https:\/\/blueportance.com\/en\/knowledge-base\/expert-guides\/understanding-pain\/\">Understanding Pain<\/a> \u2192 Neurosensory Deprogramming\n<\/nav>\n\n<div class=\"bp-bdc-header-card\">\n  <div class=\"bp-bdc-kicker\">Blue Portance Expert Guides<\/div>\n  <div class=\"bp-bdc-rule\"><\/div>\n  <div class=\"bp-bdc-dossier-title\">Understanding Pain<\/div>\n  <div class=\"bp-bdc-dossier-subtitle\">The biological, mechanical, and neurophysiological mechanisms of pain.<\/div>\n<\/div>\n\n<p class=\"bp-bdc-dossier-link\">\n  This article is part of the Expert Guide\n  <a href=\"https:\/\/blueportance.com\/en\/knowledge-base\/expert-guides\/understanding-pain\/\">\u201cUnderstanding Pain\u201d<\/a>.\n<\/p>\n\n<span class=\"bp-pillar-badge\">Reference article \u2014 Blue Portance Knowledge Base<\/span>\n\n<h1>Why Does Pain Continue When Nothing Seems to Explain It Anymore? Neurosensory Deprogramming<\/h1>\n\n<div class=\"bp-origin\">\n  <nav class=\"bp-bdc-toc\" aria-label=\"Table of contents\">\n  <h2>Table of Contents<\/h2>\n  <ul>\n      <li><a href=\"#a-l-origine-de-cette-reflexion\">Where this line of thinking comes from<\/a><\/li>\n      <li><a href=\"#1-une-question-qui-prolonge-l-article-precedent\">1. A question that follows on from the previous article<\/a><\/li>\n      <li><a href=\"#2-qu-entend-on-par-deprogrammation-neurosensorielle\">2. What is meant by neurosensory deprogramming?<\/a><\/li>\n      <li><a href=\"#3-sur-quels-mecanismes-documentes-ce-modele-s-appuie-t-il\">3. Which documented mechanisms does this model draw on?<\/a><\/li>\n      <li><a href=\"#lecture-proposee-par-le-modele-blue-portance\">The interpretation proposed by the Blue Portance model<\/a><\/li>\n      <li><a href=\"#4-en-quoi-ce-modele-se-distingue-t-il-des-mecanismes-deja-definis-dans-ce-dossier\">4. How does this model differ from the mechanisms already defined in this guide?<\/a><\/li>\n      <li><a href=\"#5-quels-indices-orientent-vers-ce-modele\">5. Which clues point toward this model?<\/a><\/li>\n      <li><a href=\"#6-quelles-approches-sont-mentionnees-dans-la-litterature\">6. Which approaches are mentioned in the literature?<\/a><\/li>\n      <li><a href=\"#7-limites-et-controverses\">7. Limitations and controversies<\/a><\/li>\n      <li><a href=\"#8-consequences-pratiques-pour-comprendre-une-situation\">8. Practical implications for understanding a situation<\/a><\/li>\n      <li><a href=\"#a-retenir\">Key takeaways<\/a><\/li>\n      <li><a href=\"#questions-frequentes\">Frequently asked questions<\/a><\/li>\n      <li><a href=\"#vous-cherchez-a-comprendre-ce-qui-entretient-vos-douleurs-en-position-assise\">Trying to understand what keeps your sitting-related pain going?<\/a><\/li>\n      <li><a href=\"#references-scientifiques\">Scientific references<\/a><\/li>\n  <\/ul>\n<\/nav>\n\n<h2 id=\"a-l-origine-de-cette-reflexion\">Where this line of thinking comes from<\/h2>\n  <p>\n    The concept of neurosensory deprogramming was passed on to us by Pierre Ivaldi, a physical therapist and\n    osteopath. For nearly thirty years, he was the director of a post-acute care and functional rehabilitation center.\n    There, he worked daily alongside surgeons, neurologists, and physical medicine and rehabilitation physicians.\n  <\/p>\n  <p>\n    Over the course of his clinical practice, Pierre Ivaldi developed the notions of neurosensory deprogramming and\n    neurosensory reprogramming. These terms describe certain changes observed in patients suffering from\n    chronic pain.\n  <\/p>\n  <p>\n    This article builds on that line of thinking. It sets these concepts in perspective in light of current\n    knowledge in pain neuroscience. To do so, it draws on the available data on central sensitization,\n    neural plasticity, engrams, and predictive coding.\n  <\/p>\n  <p>We extend our warmest thanks to him here.<\/p>\n<\/div>\n\n<div class=\"bp-bdc-epistemic\">\n  <strong>Epistemic note<\/strong> \u2014 This article presents neurosensory deprogramming as Blue Portance defines it: an interpretive functional model, built from scientific mechanisms that are documented separately (central sensitization, synaptic plasticity, fear and pain engrams), but which constitutes neither a diagnostic category recognized by the IASP nor an established scientific consensus as such. It never replaces a medical evaluation and should not be confused with neuropathic pain or nociplastic pain, which have already been defined in this guide.\n<\/div>\n\n<h3>What this article proposes<\/h3>\n\n<section class=\"bp-summary\">\n  <p>\n    <strong>Summary<\/strong> \u2014 In most people living with chronic pain, the pain remains linked to an identifiable trigger. It can, however, be amplified disproportionately by a hypersensitive nervous system. In some people, by contrast, the pain seems to gradually detach from that trigger. It then appears without any obvious mechanical factor, persists at rest, or migrates from one area to another.\n  <\/p>\n  <p>\n    In this course of events, what seems to become dysregulated would therefore not be merely a lowered triggering threshold. It would instead be the nervous system\u2019s very ability to make proper use of the sensory information it actually receives in order to adjust its response. The Blue Portance model of neurosensory deprogramming proposes an interpretation of this progressive loss of calibration. To do so, it draws on documented mechanisms: central sensitization, synaptic plasticity, and the consolidation of memory traces associated with pain (engrams). This proposed process is not presented as fixed: the same plasticity that establishes it can, at least partially, provide a way out of it.\n  <\/p>\n<\/section>\n\n<div class=\"bp-figure\">\n  <img decoding=\"async\" src=\"https:\/\/blueportance.com\/wp-content\/uploads\/VIII.1.From-Triggered-Pain-to-Autonomous-Pain.png\" alt=\"Progressive sequence from mechanically triggered pain to increasingly autonomous pain.\" loading=\"lazy\">\n<\/div>\n<p class=\"bp-figure-caption\">\n  <strong>Figure 1 \u2014 From triggered pain to autonomous pain.<\/strong> The transition to chronic pain is\n  generally a gradual process. The pain response becomes less and less dependent\n  on the initial trigger, and increasingly sustained by the nervous system\u2019s adaptation mechanisms.\n<\/p>\n\n<h2 id=\"1-une-question-qui-prolonge-l-article-precedent\">1. A question that follows on from the previous article<\/h2>\n\n<p>\n  The previous article showed how a nervous system can become hypersensitive. It then lowers its triggering threshold, amplifies signals, and spreads them beyond the initial area <span class=\"bp-inline-ref\">(Woolf, 2011)<\/span>. In that interpretation, the pain nevertheless remains tied to an identifiable trigger, even if the response is disproportionate.\n<\/p>\n\n<p>\n  One question nevertheless remains open. In some people, the pain continues to exist even though no mechanical trigger, no residual lesion, and no inflammatory context is sufficient to explain it any longer. It may thus appear at rest, at night, or move from one area of the body to another. This situation therefore does not fall under neuropathic pain, which requires a demonstrated lesion of the somatosensory system. Nor is this apparent loss of a trigger, on its own, sufficient to establish nociplastic pain in the IASP sense, even though it comes close to it <span class=\"bp-inline-ref\">(Kosek et&nbsp;al., 2016)<\/span>. It therefore raises a more specific question: why does a system that has become hypersensitive stop, in some people, depending on a trigger in order to keep producing pain?\n<\/p>\n\n<p>\n  It is precisely this question that the neurosensory deprogramming model seeks to shed light on.\n<\/p>\n\n<h2 id=\"2-qu-entend-on-par-deprogrammation-neurosensorielle\">2. What is meant by neurosensory deprogramming?<\/h2>\n\n<h3>The term, as passed on by Pierre Ivaldi<\/h3>\n\n<p>\n  In Pierre Ivaldi\u2019s clinical practice, neurosensory deprogramming refers to a change observed in\n  some patients suffering from chronic pain. The pain then gradually ceases to be tied to an\n  identifiable mechanical, postural, or lesion-related trigger, and seems to take on a form of autonomy of its own. The term\n  itself is not a diagnostic category recognized by the IASP in the way that nociceptive,\n  neuropathic, or nociplastic pain are. It is instead a clinical observation, named by its originator over the course of\n  his day-to-day work with patients in functional rehabilitation.\n<\/p>\n\n<h3>The explanatory hypothesis proposed by Blue Portance<\/h3>\n\n<div class=\"bp-definition\">\n  <strong class=\"bp-def-source\">Terminology note<\/strong>\n  <p>\n    In this article, we propose to interpret this deprogramming as a <strong>progressive loss of the\n    nervous system\u2019s ability to properly calibrate its response based on the sensory information it actually\n    receives<\/strong>. It is therefore not the body that is \u201cdeprogrammed.\u201d It is rather the mechanism that normally allows\n    the nervous system to calibrate its response to the reality of the signals it receives. This hypothesis\n    draws on biological mechanisms documented separately in the literature. It constitutes our\n    interpretation of the phenomenon described by Pierre Ivaldi, not a redefinition of the term itself.\n  <\/p>\n<\/div>\n\n<p>\n  In concrete terms, this loss of calibration corresponds to a point in the course of events at which the nervous system no longer merely\n  amplifies a signal it receives. It comes to sustain pain activity that is relatively independent of the\n  sensory information actually reaching it. This does not settle the question, still debated in the\n  literature, of whether a nervous system can produce pain that is entirely independent of any sensory\n  input <span class=\"bp-inline-ref\">(Clark, 2013)<\/span>.\n<\/p>\n\n<div class=\"bp-figure\">\n  <img decoding=\"async\" src=\"https:\/\/blueportance.com\/wp-content\/uploads\/VIII.2.Neurosensory-Reprogramming.png\" alt=\"Comparison of normal neurosensory functioning with the Blue Portance model of neurosensory deprogramming.\" loading=\"lazy\">\n<\/div>\n<p class=\"bp-figure-caption\">\n  <strong>Figure 2 \u2014 Neurosensory deprogramming.<\/strong> In the Blue Portance model, it corresponds to a\n  progressive loss of capacity. The nervous system is less and less able to make proper use of the sensory\n  information it actually receives in order to adjust its response to reality.\n<\/p>\n\n<p>\n  Understanding this hypothesis of a loss of calibration first requires revisiting the documented biological\n  mechanisms that make it plausible.\n<\/p>\n\n<h2 id=\"3-sur-quels-mecanismes-documentes-ce-modele-s-appuie-t-il\">3. Which documented mechanisms does this model draw on?<\/h2>\n\n<h3>Hyperexcitability that can become self-sustaining<\/h3>\n\n<p>\n  Central sensitization, already described in the previous article, can progress to lasting hyperexcitability of neurons in the dorsal horn of the spinal cord. Some neurons may then display spontaneous activity, independent of any current peripheral stimulation. This occurs in particular when the inhibitory mechanisms that normally dampen pain transmission become less effective <span class=\"bp-inline-ref\">(Latremoliere &amp; Woolf, 2009)<\/span>.\n<\/p>\n\n<h3>The engram concept applied to pain<\/h3>\n\n<p>\n  Among the mechanisms discussed in this article, that of engrams is receiving particular attention in the\n  recent literature. On its own, it does not constitute the explanation of the model: it supports\n  the broader hypothesis of a loss of calibration, alongside the other mechanisms presented below. An engram\n  refers to the physical trace, in neural circuits, that a learning process or an experience leaves in the nervous system.\n<\/p>\n<p>\n  In addition, recent work in animal neuroscience has shown that prefrontal circuits can store a lasting trace associating fear and pain. In mice, specifically disrupting this engram reduces established pain hypersensitivity without acting on the initial lesion <span class=\"bp-inline-ref\">(Stegemann et&nbsp;al., 2023)<\/span>. This work remains preclinical and does not support the claim that an identical mechanism explains chronic pain in humans. It nevertheless provides a plausible framework for understanding how a painful experience could, in some people, become durably consolidated in brain circuits rather than fading away.\n<\/p>\n\n<h3>The anterior cingulate cortex: shared plasticity<\/h3>\n\n<p>\n  The anterior cingulate cortex, in particular, displays forms of synaptic plasticity. These are involved both in the affective component of pain and in certain memory processes <span class=\"bp-inline-ref\">(Bliss et&nbsp;al., 2016)<\/span>. This overlap between pain circuits and memory circuits is thus today one of the most active lines of research for understanding the persistence of chronic pain.\n<\/p>\n\n<div class=\"bp-figure\">\n  <img decoding=\"async\" src=\"https:\/\/blueportance.com\/wp-content\/uploads\/VIII.4.Pain-Engrams-Traces-Stored-in-the-Nervous-System.png\" alt=\"Diagram illustrating formation, storage and possible reactivation of pain-related neural engrams.\" loading=\"lazy\">\n<\/div>\n<p class=\"bp-figure-caption\">\n  <strong>Figure 3 \u2014 Pain engrams.<\/strong> A painful experience can leave a lasting trace\n  in neural networks, one that can be reactivated even in the absence of the initial trigger.\n<\/p>\n\n<h3>Reorganization of resting-state brain networks<\/h3>\n\n<p>\n  In people with chronic low back pain, alterations in the functional connectivity of the default mode network have been reported <span class=\"bp-inline-ref\">(Baliki et&nbsp;al., 2008)<\/span>. This network comprises the circuits that are active when the brain is not engaged in a specific task. Longitudinal studies have also shown that certain characteristics of connectivity between the prefrontal cortex and the striatum, measured early on, are associated with the later risk of transition to chronic pain <span class=\"bp-inline-ref\">(Baliki et&nbsp;al., 2012)<\/span>. These findings extend the observations on the role of the limbic system already presented in connection with hypersensitization <span class=\"bp-inline-ref\">(Vachon-Presseau et&nbsp;al., 2016)<\/span>.\n<\/p>\n\n<h3>Predictive coding: a theoretical hypothesis, not an established fact<\/h3>\n\n<p>\n  Some researchers propose that the brain does not merely process sensory signals passively. It continuously generates predictions that it compares with incoming inputs, including for pain <span class=\"bp-inline-ref\">(Clark, 2013; B\u00fcchel et&nbsp;al., 2014)<\/span>. This predictive coding hypothesis thus offers an interesting theoretical framework. An expectation of pain, once sufficiently entrenched, could weigh on perception in the same way as a real signal. It is, however, one theoretical framework among others in cognitive neuroscience, and not a physiological mechanism unequivocally demonstrated for chronic pain in humans.\n<\/p>\n\n<h3>What these mechanisms suggest, taken together<\/h3>\n\n<p>\n  Taken together, these mechanisms do not demonstrate that a nervous system can produce pain completely cut off from all bodily information. They do, however, converge on a single idea. Beyond a simple lowering of the triggering threshold, something else seems to become progressively dysregulated. That something is the nervous system\u2019s ability to make proper use of the sensory information it actually receives in order to adjust its response. It is this hypothesis that the neurosensory deprogramming model sets out to explore.\n<\/p>\n\n<div class=\"bp-figure\">\n  <img decoding=\"async\" src=\"https:\/\/blueportance.com\/wp-content\/uploads\/VIII.3.The-Scientific-Foundations-of-the-Blue-Portance-Model.png\" alt=\"Four scientific mechanisms informing the Blue Portance neurosensory deprogramming model.\" loading=\"lazy\">\n<\/div>\n<p class=\"bp-figure-caption\">\n  <strong>Figure 4 \u2014 The scientific foundations of the Blue Portance model.<\/strong> The model does not rest on a\n  single mechanism, but on the integration of several processes that are now widely documented in\n  neuroscience.\n<\/p>\n\n<div class=\"bp-figure\">\n  <img decoding=\"async\" src=\"https:\/\/blueportance.com\/wp-content\/uploads\/VIII.5.How-Can-Pain-Persist-in-the-Absence-of-a-Trigger.png\" alt=\"Integrative sequence showing mechanisms that may contribute to persistent pain after the initial trigger has disappeared.\" loading=\"lazy\">\n<\/div>\n<p class=\"bp-figure-caption\">\n  <strong>Figure 5 \u2014 How pain can persist in the absence of a trigger.<\/strong> The Blue Portance model\n  shows that no single mechanism is sufficient on its own to explain this persistence. Their combination, however, can\n  sustain pain long after its initial cause has disappeared.\n<\/p>\n\n<div class=\"bp-model\">\n  <h2 id=\"lecture-proposee-par-le-modele-blue-portance\">The interpretation proposed by the Blue Portance model<\/h2>\n  <p>\n    In concrete terms, the neurosensory deprogramming model organizes these elements into three successive questions, intended to guide the analysis without taking the place of a diagnosis:\n  <\/p>\n  <ol>\n    <li><strong>The link to the trigger:<\/strong> does the pain remain tied, even disproportionately, to an identifiable mechanical or postural event, or does it seem to have become detached from it?<\/li>\n    <li><strong>The established trace:<\/strong> is there evidence pointing to lasting consolidation \u2014 long-standing pain, association with a striking emotional memory, persistent anticipation?<\/li>\n    <li><strong>The margin for recovery:<\/strong> which levers can be brought into play for this specific clinical picture? Graded exposure, mechanical variability \u2014 which reintroduces new and reliable sensory information, likely to help rebuild the link between actual stimulation and the response produced \u2014, mind-body support, medical follow-up.<\/li>\n  <\/ol>\n  <p>\n    This interpretive framework cannot establish a diagnosis. Clinical evaluation remains necessary to identify or exclude recognized pain mechanisms and other medical causes. It does, however, help frame the right questions when faced with pain that seems to have lost its link with what initially triggered it.\n  <\/p>\n<\/div>\n\n<p>\n  With this interpretation laid out, it still needs to be clearly distinguished from the mechanisms already defined in this guide \u2014 otherwise, confusion would be easy.\n<\/p>\n\n<h2 id=\"4-en-quoi-ce-modele-se-distingue-t-il-des-mecanismes-deja-definis-dans-ce-dossier\">4. How does this model differ from the mechanisms already defined in this guide?<\/h2>\n\n<p>\n  On the one hand, neuropathic pain requires a demonstrated lesion or disease of the somatosensory system. On the other hand, nociplastic pain corresponds to altered nociception without sufficient evidence of tissue or nerve damage. It is nevertheless defined by the IASP as a mechanism in its own right, regardless of how long it has been present <span class=\"bp-inline-ref\">(Kosek et&nbsp;al., 2016)<\/span>.\n<\/p>\n\n<p>\n  Neurosensory deprogramming, as proposed by Blue Portance, therefore does not replace either of these two categories and does not constitute a fourth diagnostic category. Rather, it describes an additional level of interpretation. This level applies in particular when pain \u2014 originally neuropathic, nociplastic, or mixed \u2014 seems to have gradually lost its link with an identifiable trigger. It is therefore not a competing mechanism, but a way of interpreting how already recognized mechanisms evolve over time.\n<\/p>\n\n\n<table aria-label=\"Three related notions, three levels of interpretation\">\n  <thead>\n    <tr>\n      <th>Notion<\/th>\n      <th>Status<\/th>\n      <th>What it describes<\/th>\n    <\/tr>\n  <\/thead>\n  <tbody>\n    <tr>\n      <td><strong>Nociplastic pain<\/strong> (article&nbsp;6)<\/td>\n      <td>Mechanism recognized by the IASP<\/td>\n      <td>Altered nociception, without sufficient evidence of tissue or nerve damage.<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Hypersensitization<\/strong> (article&nbsp;7)<\/td>\n      <td>Documented cross-cutting process<\/td>\n      <td>The lowering of the nervous system\u2019s alarm thresholds, which can accompany several mechanisms.<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Neurosensory deprogramming<\/strong> (this article)<\/td>\n      <td>Blue Portance interpretive model, not a medical classification<\/td>\n      <td>An interpretation of change over time, when pain seems to have lost its link with an identifiable trigger.<\/td>\n    <\/tr>\n  <\/tbody>\n<\/table>\n\n<div class=\"bp-controversy\">\n  <h3>Why not speak of numbered \u201cstages\u201d?<\/h3>\n  <p>\n    An earlier version of this content distinguished a \u201cstage 1\u201d and a \u201cstage 2.\u201d This terminology has been abandoned. It suggested a validated clinical classification, comparable to a medical severity stage \u2014 something no data can establish. The course described here is gradual and specific to each person; it does not correspond to discrete, diagnosable steps.\n  <\/p>\n<\/div>\n\n<p>\n  With this distinction made, a practical question remains: how can one recognize, in a real clinical picture, that pain has drifted away from its initial trigger?\n<\/p>\n\n<h2 id=\"5-quels-indices-orientent-vers-ce-modele\">5. Which clues point toward this model?<\/h2>\n\n<div class=\"bp-recognize\">\n  <h3>Features that, taken together, may point toward this level of interpretation<\/h3>\n  <ul>\n    <li>no identifiable mechanical, postural, or inflammatory trigger despite a careful search;<\/li>\n    <li>pain that appears or worsens at rest, including at night;<\/li>\n    <li>pain that migrates from one area to another without a consistent anatomical explanation;<\/li>\n    <li>persistence well beyond the usual healing time of an initially identified lesion;<\/li>\n    <li>frequent association with marked anticipation of pain or with generalized avoidance of movement.<\/li>\n  <\/ul>\n<\/div>\n\n<p>\n  None of these features, taken in isolation, is sufficient to reach a conclusion. As with nociplastic pain, this is a body of converging clinical evidence, not a biological test or an imaging study that allows direct confirmation.\n<\/p>\n\n<h2 id=\"6-quelles-approches-sont-mentionnees-dans-la-litterature\">6. Which approaches are mentioned in the literature?<\/h2>\n\n<p>\n  The aim here is not to propose a treatment protocol: this article is not intended to take the place of one. It\n  is rather to outline the main families of approaches discussed in the scientific literature for what Pierre Ivaldi called\n  <strong>neurosensory reprogramming<\/strong>. This term refers to the nervous system\u2019s ability to gradually rebuild\n  a response that is more accurately calibrated to the sensory information it actually receives.\n<\/p>\n\n<h3>Graded exposure below the pain threshold<\/h3>\n\n<p>\n  Stimulation that systematically triggers pain tends to confirm, for the nervous system, the association between movement and threat. Conversely, a gradual reintroduction of movements below that threshold can reduce fear of movement. This approach follows directly from the fear-avoidance model already presented in this guide <span class=\"bp-inline-ref\">(Vlaeyen &amp; Linton, 2000)<\/span>.\n<\/p>\n\n<h3>Mirror therapy and graded motor imagery<\/h3>\n\n<p>\n  These approaches, originally developed for phantom limb pain, harness the plasticity of the body\u2019s cortical representation <span class=\"bp-inline-ref\">(Ramachandran &amp; Rogers-Ramachandran, 1996; Flor et&nbsp;al., 2006)<\/span>. A controlled trial thus showed a greater reduction in pain than that achieved with standard care. It involved people with phantom limb pain or complex regional pain syndrome <span class=\"bp-inline-ref\">(Moseley, 2006)<\/span>. This result was broadly corroborated by a later systematic review covering broader chronic pain populations <span class=\"bp-inline-ref\">(Bowering et&nbsp;al., 2013)<\/span>.\n<\/p>\n\n<h3>Neurofeedback<\/h3>\n\n<p>\n  This approach aims to train a person to voluntarily modulate certain parameters of their brain activity, displayed in real time. A randomized trial in people with fibromyalgia reported an improvement in pain and in several associated symptoms. This improvement was comparable to that achieved with a standard drug treatment <span class=\"bp-inline-ref\">(Kayiran et&nbsp;al., 2010)<\/span>. The available data nevertheless remain limited in the number of studies.\n<\/p>\n\n<h3>Mechanical variability, a complementary lever<\/h3>\n\n<p>\n  As mentioned in the previous article, poor and repetitive mechanical information can help sustain a nervous system that is already hypersensitive <span class=\"bp-inline-ref\">(Langevin, 2006)<\/span>. Reintroducing postural variability therefore does not directly target a consolidated pain engram, but it may reduce one of the sources of signals likely to sustain it.\n<\/p>\n\n<p>\n  All of these approaches share one thing in common: none of them acts alone on all the levels involved. Managing this type of clinical picture therefore calls for multidisciplinary care, not a single technique applied on its own.\n<\/p>\n\n<p>\n  As with the previous articles in this guide, this interpretive framework, presented above, calls for a caveat regarding its limitations.\n<\/p>\n\n<h2 id=\"7-limites-et-controverses\">7. Limitations and controversies<\/h2>\n\n<div class=\"bp-controversy\">\n  <h3>What should not be claimed too quickly<\/h3>\n  <ul>\n    <li><strong>\u201cThis pain is disconnected from the body\u201d:<\/strong> the mechanisms discussed here remain biological; they do not mean that the pain is imaginary or has no physiological basis.<\/li>\n    <li><strong>\u201cThe brain invents the pain\u201d:<\/strong> the work on engrams and predictive coding remains, for the most part, preliminary or derived from animal models. It does not support the claim that an identical, demonstrated mechanism exists in humans.<\/li>\n    <li><strong>\u201cSince the pain is long-standing, it must have become autonomous\u201d:<\/strong> chronic pain can remain linked, in whole or in part, to an active mechanical or tissue cause. That cause must continue to be investigated.<\/li>\n    <li><strong>\u201cThis interpretation replaces medical diagnosis\u201d:<\/strong> that is never its purpose; it organizes reasoning that complements the clinical evaluation.<\/li>\n  <\/ul>\n<\/div>\n\n<p>\n  Another limitation lies in the very nature of the research field. A large part of what this model draws on \u2014 engrams, predictive coding \u2014 comes from recent, sometimes preclinical, work. On these specific points, the scientific consensus remains considerably less established than for central sensitization or the IASP definition of nociplastic pain.\n<\/p>\n\n<h2 id=\"8-consequences-pratiques-pour-comprendre-une-situation\">8. Practical implications for understanding a situation<\/h2>\n\n<ul>\n  <li><strong>Trigger:<\/strong> does the pain remain linked to an identifiable mechanical or postural factor, even if amplified?<\/li>\n  <li><strong>Timing:<\/strong> does it now appear at rest, at night, or in the absence of any load or activity?<\/li>\n  <li><strong>Distribution:<\/strong> does it migrate from one area to another without anatomical consistency?<\/li>\n  <li><strong>History:<\/strong> is there a significant emotional context associated with the onset or worsening of the pain?<\/li>\n  <li><strong>Resources:<\/strong> which levers \u2014 gradual movement, variability, specialized support \u2014 have not yet been brought into play?<\/li>\n<\/ul>\n\n<p>\n  Rapid worsening, the appearance of new neurological signs, or a decline in general health changes the picture. However long-standing the pain, these signs should prompt a medical reassessment without delay.\n<\/p>\n\n<p>\n  Neurosensory deprogramming is not presented here as an irreversible state. Plasticity mechanisms\n  allow the nervous system to gradually drift away from adaptive functioning. But this same\n  plasticity is also the biological basis of what Pierre Ivaldi called <strong>neurosensory\n  reprogramming<\/strong>. This does not correspond to an \u201cerasure\u201d of previous circuits. It is rather a\n  new, gradual learning process that allows the nervous system to rebuild a response more accurately calibrated\n  to the sensory information it receives.\n<\/p>\n\n<div class=\"bp-figure\">\n  <img decoding=\"async\" src=\"https:\/\/blueportance.com\/wp-content\/uploads\/VIII.6.Possible-Pathways-of-Neurosensory-Reprogramming.png\" alt=\"Proposed pathways for neurosensory reprogramming through reduced constraints, sensory variability and progressive movement.\" loading=\"lazy\">\n<\/div>\n<p class=\"bp-figure-caption\">\n  <strong>Figure 6 \u2014 Possible pathways to neurosensory reprogramming.<\/strong> Recovery does not generally rely\n  on a single intervention, but on the combination of several levers acting at different\n  levels of the nervous system.\n<\/p>\n\n<div class=\"bp-takeaway\">\n  <h2 id=\"a-retenir\">Key takeaways<\/h2>\n  <ul>\n    <li>In some people, chronic pain can gradually lose its link with an identifiable mechanical trigger. This is what Pierre Ivaldi named neurosensory deprogramming, based on his clinical experience.<\/li>\n    <li>Blue Portance proposes an interpretation of it, not a redefinition. It is a progressive loss of the nervous system\u2019s ability to properly calibrate its response based on the sensory information it actually receives, and it does not constitute a recognized diagnostic category.<\/li>\n    <li>It draws on separately documented mechanisms: spinal hyperexcitability, prefrontal engrams associating fear and pain, reorganization of brain networks, and the theoretical hypothesis of predictive coding.<\/li>\n    <li>This model nevertheless remains distinct from neuropathic pain and nociplastic pain as defined by the IASP.<\/li>\n    <li>No single approach is sufficient: graded exposure, mirror therapy, neurofeedback, and mechanical variability are mentioned in the literature as complementary levers, to be discussed with qualified professionals.<\/li>\n    <li>This process is not presented as irreversible. The same plasticity that establishes deprogramming is also the biological basis of neurosensory reprogramming, which makes it possible, at least partially, to move out of it.<\/li>\n  <\/ul>\n<\/div>\n\n<section class=\"bp-faq\">\n  <h2 id=\"questions-frequentes\">Frequently asked questions<\/h2>\n\n  <h3>About the model and its foundations<\/h3>\n\n  <details>\n    <summary>What is neurosensory deprogramming?<\/summary>\n    <div class=\"faq-content\">\n      It is the term used by Pierre Ivaldi, a physical therapist and osteopath, to describe a change observed in some patients suffering from chronic pain: the pain gradually ceases to be tied to an identifiable trigger. Blue Portance proposes an interpretation of it, not a redefinition: a progressive loss of the nervous system\u2019s ability to properly calibrate its response based on the sensory information it actually receives, drawing on plasticity mechanisms documented separately in the literature. It is not a diagnostic category recognized by the IASP.\n    <\/div>\n  <\/details>\n\n  <details>\n    <summary>Is this pain recognized by the international scientific community?<\/summary>\n    <div class=\"faq-content\">\n      The biological mechanisms drawn on (central sensitization, engrams, predictive coding) are individually documented, with varying degrees of certainty. Combining them into an overall explanatory model of chronic pain, however, remains an interpretation specific to Blue Portance, not an official medical classification.\n    <\/div>\n  <\/details>\n\n  <details>\n    <summary>What is an engram, as applied to pain?<\/summary>\n    <div class=\"faq-content\">\n      An engram is the physical trace that a learning process leaves in neural circuits. Recent work, mainly in animals, suggests that prefrontal circuits can store a lasting trace associating fear and pain, which may perpetuate pain perception independently of the initial lesion. It is one documented mechanism among others, not the sole explanation for neurosensory deprogramming.\n    <\/div>\n  <\/details>\n\n  <h3>About the approaches and reversibility<\/h3>\n\n  <details>\n    <summary>Is mirror therapy effective for all types of pain?<\/summary>\n    <div class=\"faq-content\">\n      It is mainly documented for phantom limb pain and complex regional pain syndrome. Its extension to other chronic pain conditions, however, rests on more limited data and should be discussed with a professional trained in this approach.\n    <\/div>\n  <\/details>\n\n  <details>\n    <summary>Can this process be reversed?<\/summary>\n    <div class=\"faq-content\">\n      The mechanisms discussed here are based on the plasticity of the nervous system, which is not a one-way street. This same plasticity is the biological basis of what Pierre Ivaldi called neurosensory reprogramming: not an erasure of previous circuits, but a new, gradual learning process. Improvement therefore remains possible in many people, but it is generally gradual and depends on the regularity of the approaches implemented, not on an isolated one-off effort.\n    <\/div>\n  <\/details>\n<\/section>\n\n<div class=\"bp-cta\">\n  <h2 id=\"vous-cherchez-a-comprendre-ce-qui-entretient-vos-douleurs-en-position-assise\">Trying to understand what keeps your sitting-related pain going?<\/h2>\n  <p>\n    The analysis is based on location, stresses, mechanical variability, and the mechanisms likely to combine.\n  <\/p>\n  <a href=\"https:\/\/blueportance.com\/en\/personalized-pain-analysis\/\">Analyze my situation \u2192<\/a>\n<\/div>\n\n<p class=\"bp-note\">\n  <strong>Note:<\/strong> this content explains general mechanisms and an interpretive model specific to Blue Portance. It cannot be used to diagnose neurosensory deprogramming remotely or to choose a treatment. Chronic pain with no identifiable trigger should be discussed with a healthcare professional.\n<\/p>\n\n<section class=\"bp-references\">\n  <h2 id=\"references-scientifiques\">Scientific references<\/h2>\n  <h3>Central sensitization, plasticity, and engrams<\/h3>\n  <ol>\n    <li>Woolf CJ. <em>Central sensitization: implications for the diagnosis and treatment of pain.<\/em> Pain. 2011;152(3 Suppl):S2\u2013S15.<\/li>\n    <li>Latremoliere A, Woolf CJ. <em>Central sensitization: a generator of pain hypersensitivity by central neural plasticity.<\/em> Journal of Pain. 2009;10(9):895\u2013926.<\/li>\n    <li>Bliss TVP, Collingridge GL, Kaang BK, Zhuo M. <em>Synaptic plasticity in the anterior cingulate cortex in acute and chronic pain.<\/em> Nature Reviews Neuroscience. 2016;17(8):485\u2013496.<\/li>\n    <li>Stegemann A, Liu S, Retana Romero OA, et al. <em>Prefrontal engrams of long-term fear memory perpetuate pain perception.<\/em> Nature Neuroscience. 2023;26(5):820\u2013829.<\/li>\n    <li>Kosek E, Cohen M, Baron R, et al. <em>Do we need a third mechanistic descriptor for chronic pain states?<\/em> Pain. 2016;157(7):1382\u20131386.<\/li>\n  <\/ol>\n  <h3>Brain reorganization and predictive coding<\/h3>\n  <ol start=\"6\">\n    <li>Baliki MN, Geha PY, Apkarian AV, Chialvo DR. <em>Beyond feeling: chronic pain hurts the brain, disrupting the default-mode network dynamics.<\/em> Journal of Neuroscience. 2008;28(6):1398\u20131403.<\/li>\n    <li>Baliki MN, Petre B, Torbey S, et al. <em>Corticostriatal functional connectivity predicts transition to chronic back pain.<\/em> Nature Neuroscience. 2012;15(8):1117\u20131119.<\/li>\n    <li>Vachon-Presseau E, Centeno MV, Ren W, et al. <em>The emotional brain as a predictor and amplifier of chronic pain.<\/em> Journal of Dental Research. 2016;95(6):605\u2013612.<\/li>\n    <li>Clark A. <em>Whatever next? Predictive brains, situated agents, and the future of cognitive science.<\/em> Behavioral and Brain Sciences. 2013;36(3):181\u2013204.<\/li>\n    <li>B\u00fcchel C, Geuter S, Sprenger C, Eippert F. <em>Placebo analgesia: a predictive coding perspective.<\/em> Neuron. 2014;81(6):1223\u20131239.<\/li>\n  <\/ol>\n  <h3>Approaches mentioned and mechanical factors<\/h3>\n  <ol start=\"11\">\n    <li>Vlaeyen JWS, Linton SJ. <em>Fear-avoidance and its consequences in chronic musculoskeletal pain: a state of the art.<\/em> Pain. 2000;85(3):317\u2013332.<\/li>\n    <li>Ramachandran VS, Rogers-Ramachandran D. <em>Synaesthesia in phantom limbs induced with mirrors.<\/em> Proceedings of the Royal Society B. 1996;263(1369):377\u2013386.<\/li>\n    <li>Flor H, Nikolajsen L, Staehelin Jensen T. <em>Phantom limb pain: a case of maladaptive CNS plasticity?<\/em> Nature Reviews Neuroscience. 2006;7(11):873\u2013881.<\/li>\n    <li>Moseley GL. <em>Graded motor imagery for pathologic pain: a randomized controlled trial.<\/em> Neurology. 2006;67(12):2129\u20132134.<\/li>\n    <li>Bowering KJ, O&#8217;Connell NE, Tabor A, et al. <em>The effects of graded motor imagery and its components on chronic pain: a systematic review and meta-analysis.<\/em> Journal of Pain. 2013;14(1):3\u201313.<\/li>\n    <li>Kayiran S, Dursun E, Dursun N, Ermutlu N, Karam\u00fcrsel S. <em>Neurofeedback intervention in fibromyalgia syndrome: a randomized, controlled, rater blind clinical trial.<\/em> Applied Psychophysiology and Biofeedback. 2010;35(4):293\u2013302.<\/li>\n    <li>Langevin HM. <em>Connective tissue: a body-wide signaling network?<\/em> Medical Hypotheses. 2006;66(6):1074\u20131077.<\/li>\n  <\/ol>\n<\/section>\n\n<p class=\"bp-copyright\">\n  \u00a9 Gil Ayache. The concepts, diagrams, terminology, and principles presented on this page constitute a work protected by copyright. They are made available to Blue Portance under an intellectual property license agreement, without transfer of economic rights or of authorship.\n<\/p>\n\n\n","protected":false},"excerpt":{"rendered":"<p>Blue Portance \u2192 Knowledge Base \u2192 Understanding Pain \u2192 Neurosensory Deprogramming Blue Portance Expert Guides Understanding Pain The biological, mechanical, and neurophysiological mechanisms of pain. This article is part of the Expert Guide \u201cUnderstanding Pain\u201d. Reference article \u2014 Blue Portance Knowledge Base Why Does Pain Continue When Nothing Seems to Explain It Anymore? 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