{"id":8022,"date":"2026-07-16T22:44:29","date_gmt":"2026-07-16T20:44:29","guid":{"rendered":"https:\/\/blueportance.com\/knowledge-base\/expert-guides\/understanding-pain\/three-pain-mechanisms\/"},"modified":"2026-10-25T22:43:22","modified_gmt":"2026-10-25T21:43:22","slug":"three-pain-mechanisms","status":"publish","type":"page","link":"https:\/\/blueportance.com\/en\/knowledge-base\/expert-guides\/understanding-pain\/three-pain-mechanisms\/","title":{"rendered":"KB 3_Expert Guide_01_Understanding Pain_02_Three Pain Mechanisms"},"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    .bp-q-breadcrumb a:hover{text-decoration:underline}\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    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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 The Three Mechanisms of Pain\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\">\n    The biological, mechanical, and neurophysiological mechanisms that explain how sitting-related pain develops and why it persists.\n  <\/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<h1>Nociceptive, Neuropathic, and Nociplastic Pain: Three Mechanisms That Can Combine<\/h1>\n\n<div class=\"bp-bdc-epistemic\">\n  <strong>Epistemic note<\/strong> \u2014 This article belongs to the \u201cUnderstanding Pain\u201d Expert Guide of the Blue Portance Knowledge Base: the concepts defined here form the foundation used throughout the Expert Guides, frequently asked questions, lived experiences, and case studies. It also distinguishes between knowledge established in the scientific literature, the biomechanical model proposed by Blue Portance, and hypotheses or clinical observations that are not yet the subject of an established consensus. Finally, it aims to explain general mechanisms and does not constitute a medical diagnosis or prescription.\n<\/div>\n\n<section class=\"bp-summary\">\n  <p>\n    Pain can arise from three main mechanisms: the activation of nociceptors by an actual or potential threat to tissues (<strong>nociceptive mechanism<\/strong>), a lesion or disease of the somatosensory nervous system (<strong>neuropathic mechanism<\/strong>), or altered nociception that cannot be sufficiently explained by the two previous mechanisms (<strong>nociplastic mechanism<\/strong>). These mechanisms are not three sealed boxes: they can coexist, change over time, and contribute in different proportions to the same pain experience.\n  <\/p>\n<\/section>\n\n<nav class=\"bp-bdc-toc\" aria-label=\"Table of contents\">\n  <h2>Table of Contents<\/h2>\n  <ul>\n      <li><a href=\"#pourquoi-cet-article-est-important\">Why this article matters<\/a><\/li>\n      <li><a href=\"#1-trois-mecanismes-pas-trois-intensites-de-douleur\">1. Three mechanisms, not three levels of pain intensity<\/a><\/li>\n      <li><a href=\"#2-le-mecanisme-nociceptif-lorsqu-une-menace-tissulaire-active-des-nocicepteurs\">2. The nociceptive mechanism: when a threat to tissue activates nociceptors<\/a><\/li>\n      <li><a href=\"#3-le-mecanisme-neuropathique-lorsque-le-systeme-somatosensoriel-est-atteint\">3. The neuropathic mechanism: when the somatosensory system is affected<\/a><\/li>\n      <li><a href=\"#4-le-mecanisme-nociplastique-lorsque-la-nociception-est-alteree\">4. The nociplastic mechanism: when nociception is altered<\/a><\/li>\n      <li><a href=\"#5-pourquoi-les-symptomes-ne-permettent-ils-pas-de-classer-seuls-la-douleur\">5. Why can\u2019t symptoms alone classify pain?<\/a><\/li>\n      <li><a href=\"#6-les-mecanismes-peuvent-ils-se-combiner\">6. Can the mechanisms combine?<\/a><\/li>\n      <li><a href=\"#7-une-douleur-peut-elle-evoluer-dans-le-temps\">7. Can pain evolve over time?<\/a><\/li>\n      <li><a href=\"#8-lecture-proposee-par-le-modele-biomecanique-blue-portance\">8. The interpretation proposed by the Blue Portance biomechanical model<\/a><\/li>\n      <li><a href=\"#9-consequences-pratiques-pour-comprendre-une-douleur\">9. Practical implications for understanding pain<\/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=\"pourquoi-cet-article-est-important\">Why this article matters<\/h2>\n\n<p>\n  The foundational article\n  <a href=\"https:\/\/blueportance.com\/en\/knowledge-base\/expert-guides\/understanding-pain\/why-do-i-hurt\/\">\u201cWhy Do I Hurt?\u201d<\/a>\n  described the general chain linking a mechanical stress, a tissue, nociception, nerve transmission, brain integration, and the pain experience. This chain explains how a signal can arise and why pain can never be reduced to a simple snapshot of a lesion.\n<\/p>\n\n<p>\n  One essential question remains, however: <strong>which mechanism is mainly driving this experience?<\/strong> The signal may come from tissues under threat, from the somatosensory system itself when it is injured or diseased, or from profoundly altered nociception without sufficient evidence of either of these mechanisms. These distinctions now structure the international terminology of pain <span class=\"bp-inline-ref\">(IASP; Raja et&nbsp;al., 2020)<\/span>, and they are also part of the chronic pain classification proposed by the IASP for the 11th revision of the International Classification of Diseases <span class=\"bp-inline-ref\">(Treede et&nbsp;al., 2019)<\/span>.\n<\/p>\n\n<p>\n  On their own, they are not enough to make a diagnosis. They do, however, provide an essential framework for avoiding several errors: believing that intense pain necessarily proves significant damage, labeling as neuropathic any pain felt along the course of a nerve, or reducing nociplastic pain to \u201cpsychological\u201d pain.\n<\/p>\n\n<div class=\"bp-recognize\">\n  <h3>Three different questions<\/h3>\n  <ul>\n    <li><strong>Nociceptive:<\/strong> are nociceptors being activated by an actual or potential threat to non-neural tissues?<\/li>\n    <li><strong>Neuropathic:<\/strong> is there a lesion or disease of the somatosensory nervous system that could explain the distribution and the signs observed?<\/li>\n    <li><strong>Nociplastic:<\/strong> does nociception appear altered, without peripheral nociceptive activation or somatosensory involvement being sufficient to explain the pain?<\/li>\n  <\/ul>\n<\/div>\n\n<h2 id=\"1-trois-mecanismes-pas-trois-intensites-de-douleur\">1. Three mechanisms, not three levels of pain intensity<\/h2>\n\n<p>\n  The terms <em>nociceptive<\/em>, <em>neuropathic<\/em>, and <em>nociplastic<\/em> do not describe how intense a pain is. Nociceptive pain can be extremely intense; neuropathic pain can remain intermittent; nociplastic pain can be localized or widespread. In reality, these terms primarily describe the <strong>biological mechanism considered to explain the pain<\/strong>.\n<\/p>\n\n<p>\n  The IASP also points out that pain and nociception are two distinct phenomena: the activity of sensory neurons alone is not enough to demonstrate or measure what a person actually experiences <span class=\"bp-inline-ref\">(IASP Terminology; Raja et&nbsp;al., 2020)<\/span>. All pain is therefore integrated by the central nervous system, but not all pain originates in the same process.\n<\/p>\n\n<figure class=\"bp-figure\">\n  <img decoding=\"async\"\n    src=\"https:\/\/blueportance.com\/wp-content\/uploads\/II.1.The-3-mechnisms-of-pain.png\"\n    alt=\"The three biological mechanisms of pain: nociceptive, neuropathic, and nociplastic.\"\n    loading=\"lazy\"\n  \/>\n  <figcaption>\n    <span class=\"bp-fig-title\">Figure 1 \u2014 The 3 mechanisms of pain<\/span>\n    <span class=\"bp-fig-text\">The nociceptive, neuropathic, and nociplastic mechanisms correspond to three distinct biological processes that can contribute, alone or in combination, to the same pain.<\/span>\n  <\/figcaption>\n<\/figure>\n\n<h2 id=\"2-le-mecanisme-nociceptif-lorsqu-une-menace-tissulaire-active-des-nocicepteurs\">2. The nociceptive mechanism: when a threat to tissue activates nociceptors<\/h2>\n\n<div class=\"bp-definition\">\n  <strong class=\"bp-def-source\">IASP terminology<\/strong>\n  <p>\n    Nociceptive pain is associated with actual or potential damage to non-neural tissue and results from the activation of nociceptors. This definition, by contrast, distinguishes it from neuropathic pain, which implies a lesion or disease of the somatosensory system.\n  <\/p>\n<\/div>\n\n<p>\n  Nociceptors are specialized sensory endings capable of transducing potentially threatening mechanical, thermal, or chemical stimuli. Their activation then produces signals transmitted to the spinal cord and supraspinal structures, where they are modulated and integrated <span class=\"bp-inline-ref\">(Basbaum et&nbsp;al., 2009; Julius, 2013)<\/span>.\n<\/p>\n\n<p>\n  In sitting-related pain, the stimulus is often mechanical: compression, traction, shear, friction, sustained deformation, or repeated stress. It may also involve a joint capsule, a ligament, an enthesis, a muscle, a tendon, fascia, the periosteum, or other innervated tissues. Local inflammation or ischemia can then sensitize nociceptors and lower their response threshold <span class=\"bp-inline-ref\">(Basbaum et&nbsp;al., 2009; Gold &amp; Gebhart, 2010)<\/span>.\n<\/p>\n\n<figure class=\"bp-figure\">\n  <img decoding=\"async\"\n    src=\"https:\/\/blueportance.com\/wp-content\/uploads\/II.2.Nociceptive-pain-how-does-it-work.png\"\n    alt=\"Diagram showing the nociceptive mechanism from mechanical stress and tissue loading to nociceptor activation, neural transmission, and pain perception.\"\n    loading=\"lazy\"\n  \/>\n  <figcaption>\n    <span class=\"bp-fig-title\">Figure 2 \u2014 Nociceptive pain: how does it work?<\/span>\n    <span class=\"bp-fig-text\">When a mechanical stress exceeds a tissue\u2019s adaptive capacity, it can activate nociceptors. The signal is then transmitted to the spinal cord and brain, where it is modulated and integrated before pain is perceived.<\/span>\n  <\/figcaption>\n<\/figure>\n\n<h3>Nociception does not mean visible damage<\/h3>\n\n<p>\n  The term <em>nociceptive<\/em> does not necessarily mean that a tear, a fracture, or an imaging abnormality must be visible. A potential threat, local inflammation, sustained deformation, or a functional disturbance can activate or sensitize nociceptors without producing a detectable macroscopic lesion. Conversely, a visible anatomical abnormality may remain painless.\n<\/p>\n\n<p>\n  This is where the notion of <strong>tissue adaptive capacity<\/strong>, developed in the foundational article, comes in: the effect of a mechanical stress depends on its intensity, but also on its duration, its repetition, the recovery available, and the condition of the tissue receiving it. This formulation is a biomechanical way of organizing the problem. It does not, however, replace the international definition of the nociceptive mechanism.\n<\/p>\n\n<h2 id=\"3-le-mecanisme-neuropathique-lorsque-le-systeme-somatosensoriel-est-atteint\">3. The neuropathic mechanism: when the somatosensory system is affected<\/h2>\n\n<div class=\"bp-definition\">\n  <strong class=\"bp-def-source\">Reference clinical definition<\/strong>\n  <p>\n    Neuropathic pain is pain caused by a lesion or disease of the somatosensory nervous system <span class=\"bp-inline-ref\">(Finnerup et&nbsp;al., 2016; IASP)<\/span>.\n  <\/p>\n<\/div>\n\n<p>\n  This definition sets an important requirement: pain felt in a nerve\u2019s distribution, pain described as burning, or pain triggered by a posture is not, on its own, proof of a neuropathic mechanism. In practice, one must look for a compatible history, an anatomically plausible distribution, and positive or negative signs suggesting somatosensory involvement <span class=\"bp-inline-ref\">(Finnerup et&nbsp;al., 2016)<\/span>.\n<\/p>\n\n<p>\n  When a nerve is injured or diseased, several phenomena can contribute to pain: ectopic discharges in sensory fibers or ganglia, changes in ion channel expression, abnormal activity at the lesion site, reorganization of spinal connections, and a reduction in certain inhibitory controls <span class=\"bp-inline-ref\">(Baron et&nbsp;al., 2010; Finnerup, Kuner &amp; Jensen, 2021)<\/span>. In concrete terms, an ectopic discharge is an electrical signal fired spontaneously by an injured nerve fiber \u2014 a bit like a stripped wire giving off sparks without any external stress being applied.\n<\/p>\n\n<h3>Why nerve compression does not automatically mean \u201cneuropathic pain\u201d<\/h3>\n\n<p>\n  A peripheral nerve is not just a cable made of axons. It includes connective sheaths, blood vessels, and a mechanical environment. Compression or tensioning may first load the sheaths and neighboring tissues, alter blood supply, or disrupt gliding. These elements can generate a nociceptive component. A neuropathic component, for its part, appears when the mechanical stress is associated with a lesion or disease of the somatosensory system that meets the accepted definition.\n<\/p>\n\n<p>\n  The two mechanisms can therefore coexist. This coexistence explains why it would be simplistic to contrast an entirely nociceptive \u201cirritated nerve\u201d with an entirely neuropathic \u201cinjured nerve\u201d as two states that are always easy to tell apart.\n<\/p>\n\n<figure class=\"bp-figure\">\n  <img decoding=\"async\"\n    src=\"https:\/\/blueportance.com\/wp-content\/uploads\/II.3.Neuropathic-pain-how-does-it-work.png\"\n    alt=\"Diagram showing neuropathic pain arising from a lesion or disease of the somatosensory nervous system and its possible coexistence with nociceptive pain.\"\n    loading=\"lazy\"\n  \/>\n  <figcaption>\n    <span class=\"bp-fig-title\">Figure 3 \u2014 Neuropathic pain: how does it work?<\/span>\n    <span class=\"bp-fig-text\">Neuropathic pain implies a lesion or disease of the somatosensory nervous system. A nociceptive component may nevertheless coexist when the nerve\u2019s sheaths, its blood vessels, or the surrounding tissues are also under load.<\/span>\n  <\/figcaption>\n<\/figure>\n\n\n<h2 id=\"4-le-mecanisme-nociplastique-lorsque-la-nociception-est-alteree\">4. The nociplastic mechanism: when nociception is altered<\/h2>\n\n<div class=\"bp-definition\">\n  <strong class=\"bp-def-source\">IASP terminology<\/strong>\n  <p>\n    Nociplastic pain arises from altered nociception, without clear evidence of actual or potential damage to non-neural tissue activating nociceptors, or of a lesion or disease of the somatosensory system explaining the pain.\n  <\/p>\n<\/div>\n\n<p>\n  The term <em>nociplastic<\/em> was introduced to address a persistent difficulty: some pain could not be adequately classified as nociceptive or neuropathic, even though the pain experience, the functional limitations, and the changes in sensitivity were real. The term was proposed in the IASP taxonomy in 2016\u20132017, and clinical criteria were subsequently developed for certain chronic musculoskeletal pain conditions <span class=\"bp-inline-ref\">(Kosek et&nbsp;al., 2016; Kosek et&nbsp;al., 2021)<\/span>.\n<\/p>\n\n<p>\n  Nociplastic pain should not be summed up as \u201cthe brain inventing pain.\u201d On the one hand, pain is always an experience produced by the nervous system; on the other, the expression <em>altered nociception<\/em> does not refer exclusively to a brain phenomenon. It may involve changes in information processing at several levels of the nociceptive system. Central sensitization is an important mechanism, but it is not a perfect synonym for nociplastic pain <span class=\"bp-inline-ref\">(Woolf, 2011; Fitzcharles et&nbsp;al., 2021; Nijs et&nbsp;al., 2023)<\/span>.\n<\/p>\n\n<figure class=\"bp-figure\">\n  <img decoding=\"async\"\n    src=\"https:\/\/blueportance.com\/wp-content\/uploads\/II.4.Nociplastic-pain-how-does-it-work.png\"\n    alt=\"Diagram showing altered nociception, increased nervous system sensitivity, signal amplification, and nociplastic pain.\"\n    loading=\"lazy\"\n  \/>\n  <figcaption>\n    <span class=\"bp-fig-title\">Figure 4 \u2014 Nociplastic pain: how does it work?<\/span>\n    <span class=\"bp-fig-text\">Nociplastic pain corresponds to altered nociception that is not sufficiently explained by peripheral nociceptive activation or by a lesion of the somatosensory system. It may also be accompanied by amplification, spreading, or insufficient modulation of pain-related information.<\/span>\n  <\/figcaption>\n<\/figure>\n\n<h3>A useful category, but not a diagnosis by default<\/h3>\n\n<p>\n  Normal imaging or the absence of an obvious lesion is not enough to conclude that a mechanism is nociplastic. Instead, the proposed criteria rely on a set of clues: chronicity, regional or multifocal distribution, hypersensitivity, associated symptoms, and the inability of nociceptive or neuropathic mechanisms to explain the overall clinical picture <span class=\"bp-inline-ref\">(Kosek et&nbsp;al., 2021)<\/span>.\n<\/p>\n\n<p>\n  Some conditions, such as fibromyalgia, are models frequently associated with this mechanism. Other situations may show a variable nociplastic component, in combination with inflammation, tissue damage, or neuropathy. The mechanism should therefore not be confused with the name of a disease.\n<\/p>\n\n<h2 id=\"5-pourquoi-les-symptomes-ne-permettent-ils-pas-de-classer-seuls-la-douleur\">5. Why can\u2019t symptoms alone classify pain?<\/h2>\n\n<p>\n  Verbal descriptions are valuable, but they are not specific. Burning can occur in neuropathic pain, but also with skin inflammation or tissue irritation. Diffuse pain may suggest a nociplastic component, but it can also result from several peripheral pain generators or from referred pain. Finally, allodynia can accompany different forms of sensitization.\n<\/p>\n\n<p>\n  That is why clinical classification systems combine several dimensions: pain history, location, anatomical distribution, triggering factors, sensory examination, available objective findings, and the overall consistency of the presumed mechanism <span class=\"bp-inline-ref\">(Finnerup et&nbsp;al., 2016; Kosek et&nbsp;al., 2021)<\/span>.\n<\/p>\n\n<table aria-label=\"Cautious comparison of the three pain mechanisms\">\n  <thead>\n    <tr>\n      <th>Question<\/th>\n      <th>Nociceptive mechanism<\/th>\n      <th>Neuropathic mechanism<\/th>\n      <th>Nociplastic mechanism<\/th>\n    <\/tr>\n  <\/thead>\n  <tbody>\n    <tr>\n      <td><strong>Core process<\/strong><\/td>\n      <td>Activation of nociceptors by an actual or potential threat to non-neural tissues.<\/td>\n      <td>Lesion or disease of the somatosensory nervous system.<\/td>\n      <td>Altered nociception not sufficiently explained by peripheral nociceptive activation or somatosensory involvement.<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Possible clues<\/strong><\/td>\n      <td>Notably, a reproducible link with a load, pressure, movement, inflammation, or a plausible tissue area.<\/td>\n      <td>In particular, a neuroanatomically plausible distribution, positive or negative sensory symptoms, or signs compatible with somatosensory involvement.<\/td>\n      <td>More widespread hypersensitivity, disproportion or variability, associated symptoms, nociceptive and neuropathic mechanisms insufficient to explain the overall picture.<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>What is not enough<\/strong><\/td>\n      <td>Pain that is localized or provoked by movement.<\/td>\n      <td>Burning, radiating pain, or the anatomical proximity of a nerve.<\/td>\n      <td>Normal imaging, how long the pain has lasted, or the presence of psychological stress.<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Overlap<\/strong><\/td>\n      <td colspan=\"3\">All three mechanisms can contribute simultaneously to the same pain situation.<\/td>\n    <\/tr>\n  <\/tbody>\n<\/table>\n\n<h2 id=\"6-les-mecanismes-peuvent-ils-se-combiner\">6. Can the mechanisms combine?<\/h2>\n\n<p>\n  Yes. Publications on pain mechanisms emphasize that the categories are useful for reasoning, but that real-world clinical presentations are often mixed <span class=\"bp-inline-ref\">(Fitzcharles et&nbsp;al., 2021; Finnerup, Kuner &amp; Jensen, 2021)<\/span>.\n<\/p>\n\n<figure class=\"bp-figure\">\n  <img decoding=\"async\"\n    src=\"https:\/\/blueportance.com\/wp-content\/uploads\/II.5.The-3-mechanisms-are-not-separate-boxes.png\"\n    alt=\"Diagram showing that nociceptive, neuropathic, and nociplastic mechanisms can coexist and contribute in different proportions to the same pain.\"\n    loading=\"lazy\"\n  \/>\n  <figcaption>\n    <span class=\"bp-fig-title\">Figure 5 \u2014 The 3 mechanisms are not separate boxes<\/span>\n    <span class=\"bp-fig-text\">The same pain can involve several biological mechanisms. Their relative contribution may therefore vary depending on the person, the context, and the stage of its course.<\/span>\n  <\/figcaption>\n<\/figure>\n\n<p>\n  Osteoarthritis may combine nociceptive activation from joint tissues with more widespread changes in sensitivity. Likewise, radiculopathy may bring together a nociceptive component arising from spinal structures and a neuropathic component related to nerve root involvement. Finally, chronic pelvic pain may combine tissue stress, documented nerve involvement, and progressively altered nociception.\n<\/p>\n\n<h3>The example of pudendal neuralgia<\/h3>\n\n<p>\n  Pain felt in the pudendal distribution illustrates particularly well the need to distinguish between levels. Pressure or traction in the pelvic region can load muscles, ligaments, fascia, the nerve\u2019s sheaths, and its blood vessels: these structures may contribute to a nociceptive component. If a lesion or disease of the somatosensory system is established, a neuropathic component may be considered. If the pain persists with hypersensitivity that goes beyond what these mechanisms explain, a nociplastic component may also be discussed.\n<\/p>\n\n<p>\n  This interpretation does not mean that every case of pudendal neuralgia necessarily follows this sequence. It simply shows that the same clinical diagnosis can encompass different mechanistic contributions, which partly explains the diversity of experiences and of reactions to sitting.\n<\/p>\n\n<h2 id=\"7-une-douleur-peut-elle-evoluer-dans-le-temps\">7. Can pain evolve over time?<\/h2>\n\n<p>\n  The three mechanisms are not three fixed compartments: in certain documented situations, prolonged mechanical stress can, step by step, shift the respective contribution of each mechanism. For example, persistent nociception can promote peripheral sensitization of nociceptors; if the nerve structure itself eventually becomes affected, a neuropathic component may appear; prolonged central sensitization may, in some cases, contribute to the development of a nociplastic component <span class=\"bp-inline-ref\">(Woolf, 2011; Latremoliere &amp; Woolf, 2009)<\/span>.\n<\/p>\n\n<figure class=\"bp-figure\">\n  <img decoding=\"async\"\n    src=\"https:\/\/blueportance.com\/wp-content\/uploads\/II.6.Pain-can-evolve-a-dynamic-continuum.png\"\n    alt=\"Diagram showing a possible evolution from repeated mechanical stress to persistent nociception, nerve involvement, sensitization, and a nociplastic component.\"\n    loading=\"lazy\"\n  \/>\n  <figcaption>\n    <span class=\"bp-fig-title\">Figure 6 \u2014 Pain can evolve: a dynamic continuum<\/span>\n    <span class=\"bp-fig-text\">In some situations, the contribution of each mechanism may change over time. This trajectory is, however, neither systematic nor linear: each stage may be absent, stabilized, or partially reversible.<\/span>\n  <\/figcaption>\n<\/figure>\n\n<p>\n  This dynamic reading complements, without replacing, the classification by dominant mechanism presented above: it explains why the same pain can be described differently depending on the point in its course, and why the <a href=\"https:\/\/blueportance.com\/en\/knowledge-base\/expert-guides\/understanding-pain\/\">rest of this guide<\/a> devotes separate articles to each of these mechanisms.\n<\/p>\n\n<div class=\"bp-controversy\">\n  <h3>Current controversies and limitations<\/h3>\n  <p>\n    The boundaries between mechanisms remain imperfect. There is no single biomarker that can automatically assign a pain to a category. Clinical criteria therefore provide levels of probability and must be interpreted in context.\n  <\/p>\n  <ul>\n    <li>The presence of peripheral nociception is difficult to measure directly in a person.<\/li>\n    <li>Likewise, small fiber involvement may go undetected by standard neurophysiological testing.<\/li>\n    <li>Central sensitization can accompany nociceptive or neuropathic pain without being sufficient to reclassify it as nociplastic.<\/li>\n    <li>In addition, the exact status of certain conditions varies from person to person and depending on the stage of their course.<\/li>\n    <li>Finally, biological, psychological, and social mechanisms interact, without this interaction invalidating the mechanistic distinction.<\/li>\n  <\/ul>\n  <p>\n    These limitations justify cautious wording: one often speaks of a <strong>dominant mechanism<\/strong>, a <strong>component<\/strong>, or a <strong>probability<\/strong>, rather than absolute and definitive membership in a category.\n  <\/p>\n<\/div>\n\n<div class=\"bp-model\">\n  <h2 id=\"8-lecture-proposee-par-le-modele-biomecanique-blue-portance\">8. The interpretation proposed by the Blue Portance biomechanical model<\/h2>\n\n  <p>\n    The international classification mainly answers the question: <strong>which mechanism explains the pain?<\/strong> The Blue Portance biomechanical model, for its part, proposes adding a second question: <strong>how have mechanical stresses, tissues, and the nervous system interacted over time to produce the current situation?<\/strong>\n  <\/p>\n\n  <p>\n    This interpretation builds on the chain presented in <a href=\"https:\/\/blueportance.com\/en\/knowledge-base\/expert-guides\/understanding-pain\/why-do-i-hurt\/\">Figure 1 of the article \u201cWhy Do I Hurt?\u201d<\/a>:\n  <\/p>\n\n  <blockquote>\n    mechanical stress \u2192 tissue and adaptive capacity \u2192 nociceptive activity or nerve disturbance \u2192 transmission and modulation \u2192 integration \u2192 pain \u2192 behavior \u2192 adaptation.\n  <\/blockquote>\n\n  <p>\n    From this perspective, the three mechanisms are not treated as three fixed identities, but as three possible <strong>modes of contribution<\/strong>:\n  <\/p>\n\n  <ul>\n    <li><strong>Nociceptive contribution:<\/strong> mechanical stresses load tissues and activate their nociceptors.<\/li>\n    <li><strong>Neuropathic contribution:<\/strong> the somatosensory system is itself injured or diseased and produces pathological activity.<\/li>\n    <li><strong>Nociplastic contribution:<\/strong> nociception is persistently altered in a way that the two previous mechanisms can no longer sufficiently explain.<\/li>\n  <\/ul>\n\n  <p>\n    Persistent nociceptive pain does not automatically lead to neuropathy, and neuropathy does not automatically lead to nociplastic pain. However, sustained stimulation can promote sensitization phenomena, and several mechanisms may end up intertwined. The trajectory should therefore be studied as a conditional possibility, never as a universal sequence.\n  <\/p>\n\n  <p>\n    In short, the aim is less to create a new classification than to connect the existing classification to three dimensions that are often considered separately: <strong>the nature of the mechanical stress, the adaptive capacity of the structures, and time course<\/strong>.\n  <\/p>\n<\/div>\n\n<h2 id=\"9-consequences-pratiques-pour-comprendre-une-douleur\">9. Practical implications for understanding pain<\/h2>\n\n<p>\n  Identifying a mechanism is not the same as assigning a definitive label. It is a way of organizing the questions.\n<\/p>\n\n<ul>\n  <li>\n    A <strong>nociceptive<\/strong> hypothesis leads to asking which tissues are being loaded, by what mechanical stress, for how long, and with what possibility of recovery and variation.\n  <\/li>\n  <li>\n    A <strong>neuropathic<\/strong> hypothesis likewise leads to looking for somatosensory system involvement, a neuroanatomically consistent distribution, and changes in sensory function.\n  <\/li>\n  <li>\n    A <strong>nociplastic<\/strong> hypothesis leads to examining whether nociception appears altered beyond what the identified tissue or nerve damage explains, without drawing conclusions from the mere absence of a visible abnormality.\n  <\/li>\n  <li>\n    A <strong>mixed<\/strong> hypothesis helps prevent one real mechanism from masking the others: a visible lesion does not necessarily explain all the pain, but sensitization does not cancel out the existence of a peripheral mechanical stress either.\n  <\/li>\n<\/ul>\n\n<p>\n  This method also helps interpret time course. Pain that appears immediately on contact, pain that gradually increases with sitting time, pain accompanied by sensory deficits, and pain that has become diffuse or unpredictable do not tell the same story. None of these profiles is enough on its own to establish a mechanism, but each one guides the investigation.\n<\/p>\n\n<div class=\"bp-takeaway\">\n  <h2 id=\"a-retenir\">Key takeaways<\/h2>\n  <ul>\n    <li>The terms nociceptive, neuropathic, and nociplastic describe mechanisms, not levels of intensity.<\/li>\n    <li>Nociceptive pain involves the activation of nociceptors by an actual or potential threat to non-neural tissues.<\/li>\n    <li>Neuropathic pain, likewise, implies a lesion or disease of the somatosensory nervous system.<\/li>\n    <li>Nociplastic pain corresponds to altered nociception that is not sufficiently explained by the two previous mechanisms.<\/li>\n    <li>Burning, radiating pain, or normal imaging are not enough to classify a pain.<\/li>\n    <li>In addition, the mechanisms can coexist and their relative contribution may change over time, without following a mandatory sequence.<\/li>\n    <li>Finally, the Blue Portance model proposes connecting these mechanisms to the nature of mechanical stresses, adaptive capacity, and time course.<\/li>\n  <\/ul>\n<\/div>\n\n<section class=\"bp-faq\">\n  <h2 id=\"questions-frequentes\">Frequently asked questions<\/h2>\n\n  <details>\n    <summary>Can pain be both nociceptive and neuropathic?<\/summary>\n    <div class=\"faq-content\">\n      Yes. A mechanical stress applied near a nerve can activate the nociceptors of its sheaths, its blood vessels, or the surrounding tissues, while involvement of the somatosensory nervous system can simultaneously produce a neuropathic component.\n    <\/div>\n  <\/details>\n\n  <details>\n    <summary>Does a burning sensation prove neuropathic pain?<\/summary>\n    <div class=\"faq-content\">\n      No. The quality of the sensation is a clue, but it is not specific. Burning can also accompany inflammation or tissue irritation. The anatomical distribution, sensory examination, and clinical history must be taken into account.\n    <\/div>\n  <\/details>\n\n  <details>\n    <summary>Does nociplastic pain mean the pain is psychological?<\/summary>\n    <div class=\"faq-content\">\n      No. The term describes altered nociception that is not sufficiently explained by peripheral nociceptive activation or by a lesion of the somatosensory system. Psychological and social factors can modulate any pain, but they do not make the experience imaginary.\n    <\/div>\n  <\/details>\n\n  <details>\n    <summary>Does a normal MRI mean the pain is nociplastic?<\/summary>\n    <div class=\"faq-content\">\n      No. Imaging does not show every functional, tissue, or nerve phenomenon. For this reason, nociplastic pain is not a category assigned automatically when routine diagnostic testing is normal.\n    <\/div>\n  <\/details>\n\n  <details>\n    <summary>Are the three mechanisms three successive stages?<\/summary>\n    <div class=\"faq-content\">\n      No. They may follow one another in some cases, but this progression is neither mandatory nor universal. Pain may remain mainly nociceptive, be neuropathic from the outset, present a nociplastic component, or combine several mechanisms.\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    Analyzing pain does not rest solely on its name or location, but on the mechanical stresses, the time course, the structures involved, and the mechanisms that may 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 of pain. It therefore cannot determine remotely the mechanism of an individual\u2019s pain and does not replace the advice of a healthcare professional.\n<\/p>\n\n<section class=\"bp-references\">\n  <h2 id=\"references-scientifiques\">Scientific references<\/h2>\n\n  <h3>Terminology and classification<\/h3>\n  <ol>\n    <li>\n      International Association for the Study of Pain (IASP).\n      <em>IASP Terminology \u2014 Pain Definition.<\/em> 2020.\n      <a href=\"https:\/\/www.iasp-pain.org\/resources\/terminology\/\" target=\"_blank\" rel=\"noopener\">Official terminology<\/a>.\n    <\/li>\n    <li>\n      Raja SN, Carr DB, Cohen M, et al.\n      <em>The revised International Association for the Study of Pain definition of pain: concepts, challenges and compromises.<\/em>\n      Pain. 2020;161(9):1976\u20131982. doi:10.1097\/j.pain.0000000000001939.\n    <\/li>\n    <li>\n      Treede RD, Rief W, Barke A, et al.\n      <em>Chronic pain as a symptom or a disease: the IASP Classification of Chronic Pain for the International Classification of Diseases (ICD-11).<\/em>\n      Pain. 2019;160(1):19\u201327.\n    <\/li>\n  <\/ol>\n\n  <h3>Nociceptive and neuropathic mechanisms<\/h3>\n  <ol start=\"4\">\n    <li>\n      Basbaum AI, Bautista DM, Scherrer G, Julius D.\n      <em>Cellular and molecular mechanisms of pain.<\/em>\n      Cell. 2009;139(2):267\u2013284. doi:10.1016\/j.cell.2009.09.028.\n    <\/li>\n    <li>\n      Julius D.\n      <em>TRP channels and pain.<\/em>\n      Annual Review of Cell and Developmental Biology. 2013;29:355\u2013384.\n    <\/li>\n    <li>\n      Gold MS, Gebhart GF.\n      <em>Nociceptor sensitization in pain pathogenesis.<\/em>\n      Nature Medicine. 2010;16(11):1248\u20131257.\n    <\/li>\n    <li>\n      Finnerup NB, Haroutounian S, Kamerman P, et al.\n      <em>Neuropathic pain: an updated grading system for research and clinical practice.<\/em>\n      Pain. 2016;157(8):1599\u20131606. doi:10.1097\/j.pain.0000000000000492.\n    <\/li>\n    <li>\n      Baron R, Binder A, Wasner G.\n      <em>Neuropathic pain: diagnosis, pathophysiological mechanisms, and treatment.<\/em>\n      Lancet Neurology. 2010;9(8):807\u2013819.\n    <\/li>\n    <li>\n      Finnerup NB, Kuner R, Jensen TS.\n      <em>Neuropathic pain: from mechanisms to treatment.<\/em>\n      Physiological Reviews. 2021;101(1):259\u2013301. doi:10.1152\/physrev.00045.2019.\n    <\/li>\n  <\/ol>\n\n  <h3>Nociplastic mechanism and central sensitization<\/h3>\n  <ol start=\"10\">\n    <li>\n      Kosek E, Cohen M, Baron R, et al.\n      <em>Do we need a third mechanistic descriptor for chronic pain states?<\/em>\n      Pain. 2016;157(7):1382\u20131386.\n    <\/li>\n    <li>\n      Kosek E, Cohen M, Baron R, et al.\n      <em>Chronic nociplastic pain affecting the musculoskeletal system: clinical criteria and grading system.<\/em>\n      Pain. 2021;162(11):2629\u20132634. doi:10.1097\/j.pain.0000000000002324.\n    <\/li>\n    <li>\n      Fitzcharles MA, Cohen SP, Clauw DJ, Littlejohn G, Usui C, H\u00e4user W.\n      <em>Nociplastic pain: towards an understanding of prevalent pain conditions.<\/em>\n      Lancet. 2021;397(10289):2098\u20132110. doi:10.1016\/S0140-6736(21)00392-5.\n    <\/li>\n    <li>\n      Woolf CJ.\n      <em>Central sensitization: implications for the diagnosis and treatment of pain.<\/em>\n      Pain. 2011;152(3 Suppl):S2\u2013S15. doi:10.1016\/j.pain.2010.09.030.\n    <\/li>\n    <li>\n      Latremoliere A, Woolf CJ.\n      <em>Central sensitization: a generator of pain hypersensitivity by central neural plasticity.<\/em>\n      Journal of Pain. 2009;10(9):895\u2013926.\n    <\/li>\n    <li>\n      Nijs J, Malfliet A, Nishigami T.\n      <em>Nociplastic pain and central sensitization in patients with chronic pain conditions: a terminology update for clinicians.<\/em>\n      Brazilian Journal of Physical Therapy. 2023;27(3):100518.\n    <\/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 The Three Mechanisms of Pain Blue Portance Expert Guides Understanding Pain The biological, mechanical, and neurophysiological mechanisms that explain how sitting-related pain develops and why it persists. This article is part of the Expert Guide \u201cUnderstanding Pain\u201d. Nociceptive, Neuropathic, and Nociplastic Pain: Three Mechanisms That Can [&#8230;]\n","protected":false},"author":6,"featured_media":0,"parent":8012,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_acf_changed":false,"_yoast_wpseo_title":"Three Pain Mechanisms That Can Combine | Blue Portance","_yoast_wpseo_metadesc":"Nociceptive, neuropathic, nociplastic: the three pain mechanisms recognized by the IASP and why they often combine.","footnotes":""},"pathologie_secondaire":[],"effet_positif":[],"class_list":["post-8022","page","type-page","status-publish","hentry"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO Premium plugin v28.7 (Yoast SEO v28.7) - https:\/\/yoast.com\/product\/yoast-seo-premium-wordpress\/ -->\n<title>Three Pain Mechanisms That Can Combine | Blue Portance<\/title>\n<meta name=\"description\" content=\"Nociceptive, neuropathic, nociplastic: the three pain mechanisms recognized by the IASP and why they 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