{"id":8015,"date":"2026-07-13T09:54:43","date_gmt":"2026-07-13T07:54:43","guid":{"rendered":"https:\/\/blueportance.com\/knowledge-base\/understanding-pain\/why-do-i-hurt\/"},"modified":"2026-10-25T22:43:21","modified_gmt":"2026-10-25T21:43:21","slug":"why-do-i-hurt","status":"publish","type":"page","link":"https:\/\/blueportance.com\/en\/knowledge-base\/expert-guides\/understanding-pain\/why-do-i-hurt\/","title":{"rendered":"KB 3_Expert Guide_01_Understanding Pain_01_Why Do I Hurt"},"content":{"rendered":"\n\n<!-- BDC \u2014 Understanding Pain \u2014 Chapter 1: Why Do I Hurt? \u2014 Blue Portance -->\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    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24px;padding:15px 18px;border-left:4px solid #d39b22;border-radius:6px;background:#fff8e1;color:#5a4a00;font-size:.9rem}\n    @media(max-width:640px){body{padding:16px}h1{font-size:1.5rem}}\n    .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\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 Why Do I Hurt?\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 the onset and persistence of sitting-related pain.\n  <\/div>\n<\/div>\n\n<p class=\"bp-bdc-dossier-link\">This article is part of the <a href=\"https:\/\/blueportance.com\/en\/knowledge-base\/expert-guides\/understanding-pain\/\">\u201cUnderstanding Pain\u201d<\/a> Expert Guide.<\/p>\n\n<span class=\"bp-pillar-badge\">Foundational article \u2014 Blue Portance Knowledge Base<\/span>\n\n<h1>Why Do I Hurt? Understanding the Mechanism of Pain<\/h1>\n\n<div class=\"bp-bdc-epistemic\">\n  <strong>Epistemic note<\/strong> \u2014 This article is the foundational document of the Blue Portance Knowledge Base: the concepts defined here form the groundwork used across all the Expert Guides, frequently asked questions, lived experiences, and case studies. It 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. It aims to explain general mechanisms and does not constitute a diagnosis or a medical prescription.\n<\/div>\n\n<!-- IMMEDIATE ANSWER -->\n<section class=\"bp-summary\">\n  <p>\n    Pain is not direct proof of damaged tissue. It arises when a stress exceeds the\n    <strong>adaptive capacity<\/strong> of a tissue: ligament, enthesis, muscle, fascia, or nerve. Specialized receptors\n    (nociceptors) are then activated, and this signal, transmitted to the spinal cord and then to the brain, is integrated and interpreted there.\n    This pathway explains three essential things. First, pain can appear without any lesion visible on diagnostic testing. Second, it can\n    depend as much on the <strong>duration<\/strong> of the stress as on its intensity. Finally, it can be felt in a location\n    different from the structure that actually triggered the signal.\n  <\/p>\n<\/section>\n\n<!-- INTRODUCTION \u2014 universal hook -->\n<nav class=\"bp-bdc-toc\" aria-label=\"Table of contents\">\n  <h2>Contents<\/h2>\n  <ul>\n      <li><a href=\"#une-experience-universelle\">A universal experience<\/a><\/li>\n      <li><a href=\"#a-quoi-sert-la-douleur\">What is pain for?<\/a><\/li>\n      <li><a href=\"#qu-est-ce-que-la-douleur-precisement\">What exactly is pain?<\/a><\/li>\n      <li><a href=\"#douleur-et-souffrance-deux-realites-differentes\">Pain and suffering: two different realities<\/a><\/li>\n      <li><a href=\"#quels-tissus-declenchent-reellement-la-douleur\">Which tissues actually trigger pain?<\/a><\/li>\n      <li><a href=\"#de-la-contrainte-a-la-douleur-une-chaine-pas-un-raccourci\">From stress to pain: a chain, not a shortcut<\/a><\/li>\n      <li><a href=\"#pourquoi-la-duree-change-tout\">Why duration changes everything<\/a><\/li>\n      <li><a href=\"#une-dissociation-essentielle-ou-j-ai-mal-n-est-pas-toujours-la-ou-ca-vient\">An essential dissociation: where it hurts is not always where it comes from<\/a><\/li>\n      <li><a href=\"#puis-je-avoir-mal-sans-cause-apparente\">Can I be in pain without an apparent cause?<\/a><\/li>\n      <li><a href=\"#pourquoi-certaines-douleurs-deviennent-elles-chroniques\">Why does some pain become chronic?<\/a><\/li>\n      <li><a href=\"#ce-que-cela-ne-veut-pas-dire\">What this does not mean<\/a><\/li>\n      <li><a href=\"#a-retenir\">Key takeaways<\/a><\/li>\n      <li><a href=\"#pour-aller-plus-loin\">Further reading<\/a><\/li>\n      <li><a href=\"#questions-frequentes-associees\">Related frequently asked questions<\/a><\/li>\n      <li><a href=\"#vous-reconnaissez-votre-situation\">Do you recognize your situation?<\/a><\/li>\n      <li><a href=\"#references-scientifiques\">Scientific references<\/a><\/li>\n  <\/ul>\n<\/nav>\n\n<h2 id=\"une-experience-universelle\">A universal experience<\/h2>\n<p>\n  When I get stung or put my hand on a hot plate, I instinctively understand why I\n  feel pain. The same is true when I take a blow or fall on my backside. I then feel a\n  burning sensation, a dull ache, or a pulling sensation whose cause is immediately understandable. In these\n  situations, there is an identifiable event that seems to explain the pain.\n<\/p>\n<p>\n  But what happens when pain appears without any impact, without any burn, without any visible injury, and sometimes even without\n  any abnormality found on diagnostic testing? Why can simply sitting gradually become painful?\n  Why do some people feel burning, an electric shock, or a sensation of compression even though\n  no obvious lesion is found? And above all: how can pain be felt in a location\n  different from where the problem actually lies?\n<\/p>\n<p>\n  To answer these questions, we first need to understand what pain really is \u2014 and, before that, what it is for.\n<\/p>\n\n<!-- WHAT IS PAIN FOR -->\n<h2 id=\"a-quoi-sert-la-douleur\">What is pain for?<\/h2>\n<p>\n  Before it is a problem, pain is a <strong>protective mechanism<\/strong>. It alerts the body when a tissue\n  is at risk of being damaged, or when it detects a potentially dangerous situation. Without pain, we would keep\n  loading weakened tissues without realizing it: it is therefore an alarm system essential to survival.\n<\/p>\n<p>\n  Like any alarm system, however, it can become oversensitive, persist after the initial danger has gone, or\n  react out of proportion to the actual situation.\n<\/p>\n\n<!-- WHAT IS PAIN -->\n<h2 id=\"qu-est-ce-que-la-douleur-precisement\">What exactly is pain?<\/h2>\n<div class=\"bp-definition\">\n  <strong class=\"bp-def-source\">International Association for the Study of Pain (IASP)<\/strong>\n  <p>\n    \u201cAn unpleasant sensory and emotional experience associated with, or resembling that associated with, actual\n    or potential tissue damage.\u201d <em>(Raja et al., 2020 \u2014 IASP)<\/em>\n  <\/p>\n<\/div>\n<p>\n  This definition is important: it shows that pain is not simply a signal mechanically sent by a tissue\n  to the brain. It is an <strong>experience constructed<\/strong> by the nervous system from many pieces of information:\n  the signals coming from the tissues, their biological context, and their mechanical environment. The state of the nervous system, as well as\n  the emotional and cognitive context, also contribute to it.\n<\/p>\n<p>\n  <strong>Constructed does not mean imaginary.<\/strong> It means that pain results from the nervous system\u2019s\n  interpretation of very real information. Pain is therefore never solely \u201cin the tissue,\u201d but it is not\n  solely \u201cin the head\u201d either. Rather, it results from an interaction between these different levels, and it remains, in all\n  cases, a real experience for the person who feels it.\n<\/p>\n<p>The IASP notably distinguishes two major components of this experience:<\/p>\n<ul>\n  <li><strong>The sensory (discriminative) component<\/strong> \u2014 it provides information about the location, nature, and intensity of the pain: burning, electric shock, heaviness, pulling. It is, in a sense, the pain of the body.<\/li>\n  <li><strong>The emotional component<\/strong> \u2014 the unpleasant affect that pain generates, the worry it causes, and the anticipation or avoidance behaviors it leads to. It is the pain of the mind.<\/li>\n<\/ul>\n\n<!-- THREE MECHANISMS, INTRODUCED UPFRONT -->\n<div class=\"bp-recognize\">\n  <h3>Three mechanisms that produce pain<\/h3>\n  <p>\n    Before going into detail, it is useful to know that pain can result from three main mechanisms, which are not\n    mutually exclusive. The <strong>nociceptive<\/strong> mechanism corresponds to the activation of nociceptors by tissue stress.\n    Damage to or a disturbance of the somatosensory nervous system itself defines the <strong>neuropathic<\/strong> mechanism.\n    As for the <strong>nociplastic<\/strong> mechanism, it corresponds to altered processing of pain information, without any demonstrated\n    lesion or nerve damage.\n  <\/p>\n  <p>\n    The article <a href=\"https:\/\/blueportance.com\/en\/knowledge-base\/expert-guides\/understanding-pain\/three-pain-mechanisms\/\">\u201cNociceptive, Neuropathic,\n    and Nociplastic Pain\u201d<\/a> describes each of these mechanisms in detail, along with their boundaries, their possible\n    overlaps, and concrete illustrations.\n  <\/p>\n<\/div>\n\n<!-- PAIN VS SUFFERING -->\n<h2 id=\"douleur-et-souffrance-deux-realites-differentes\">Pain and suffering: two different realities<\/h2>\n<p>\n  <strong>Pain<\/strong> is a biological signal. <strong>Suffering<\/strong> corresponds to what this signal produces\n  in the person\u2019s life: worry, limitation of activities, fatigue, loss of confidence, isolation. Both are\n  real. But they do not arise from exactly the same mechanisms \u2014 and this is, in fact, the distinction partly covered\n  by the emotional component mentioned in the IASP definition. Understanding this difference avoids reducing a person\u2019s entire\n  life to their pain signal alone, while taking seriously what they are going through.\n<\/p>\n\n<!-- WHICH TISSUES -->\n<h2 id=\"quels-tissus-declenchent-reellement-la-douleur\">Which tissues actually trigger pain?<\/h2>\n<p>\n  When we talk about pain in the tailbone, the perineum, or the sitting bones, we often imagine that it is the bone that hurts. In\n  reality, bone is rarely the painful structure. It is mainly the surrounding <strong>living tissues<\/strong>,\n  rich in sensory receptors, that can trigger a pain signal when they are loaded beyond their\n  adaptive capacity. Depending on the situation, these may include:\n<\/p>\n<ul>\n  <li>a joint <strong>capsule<\/strong>;<\/li>\n  <li>a <strong>ligament<\/strong>;<\/li>\n  <li>an <strong>enthesis<\/strong> (the area where a tendon or muscle attaches to bone);<\/li>\n  <li>a <strong>fascia<\/strong>;<\/li>\n  <li>a <strong>muscle<\/strong> or a <strong>tendon<\/strong>;<\/li>\n  <li>an <strong>intervertebral disc<\/strong>;<\/li>\n  <li>a <strong>nerve structure<\/strong>;<\/li>\n  <li>more rarely, the <strong>bone itself<\/strong>, when there is genuine bone involvement (a fracture, for example).<\/li>\n<\/ul>\n<p>\n  These tissues do not all have the same <strong>adaptive capacity<\/strong>. This is why the same stress can be\n  perfectly well tolerated by some tissues while it becomes painful for others: each tissue has its\n  own mechanical properties and its own sensitivity. This point is essential, because a single pelvic movement can\n  load several tissues at once. One of them can then become the main pain generator, without the others\n  necessarily being involved.\n<\/p>\n<p>\n  Depending on the situation, pain can result from <strong>compression<\/strong>, <strong>stretching<\/strong>,\n  <strong>shear<\/strong>, or <strong>friction<\/strong>. It can also stem from a loss of <strong>gliding<\/strong> between two tissues\n  or from excessive <strong>traction<\/strong> on an attachment. So it is not only the tissue involved that matters,\n  but also the nature of the stress it is subjected to.\n<\/p>\n\n<!-- NOCICEPTIVE CHAIN -->\n<h2 id=\"de-la-contrainte-a-la-douleur-une-chaine-pas-un-raccourci\">From stress to pain: a chain, not a shortcut<\/h2>\n<p>\n  Contrary to a very widespread belief, mechanical stress never directly produces pain. It first acts\n  on a tissue. That tissue has its own <strong>adaptive capacity<\/strong>: its ability, at any given moment, to\n  absorb this stress without damage and without an alarm signal. As long as the stress stays within the limits of this capacity,\n  nothing happens consciously.\n<\/p>\n<p>\n  When the stress exceeds this adaptive capacity, the tissue\u2019s <strong>nociceptors<\/strong> are activated: these are specialized\n  sensory receptors capable of detecting a potential threat to its integrity. They then transmit\n  information to the spinal cord and then to the brain, which <strong>integrates and interprets<\/strong> it in its\n  context. It is this interpretation that can produce the experience we call pain.\n<\/p>\n<h3>What this chain explains<\/h3>\n<p>\n  This chain explains why the same stress can be perfectly well tolerated by one person and painful for\n  another. The difference does not lie in the stress itself, but in the adaptive capacity of the tissue that\n  receives it, at that precise moment. Figure 3 then illustrates how this chain naturally unfolds depending on whether the tissues\u2019 adaptive\n  capacity is preserved or exceeded.\n<\/p>\n<p>\n  It is this mechanism \u2014 the activation of nociceptors by a stress that exceeds a tissue\u2019s adaptive capacity \u2014 that\n  is called <strong>nociceptive pain<\/strong>. It accounts for the majority of sitting-related pain.\n<\/p>\n\n<h3>The chain in a diagram<\/h3>\n<figure class=\"bp-figure\">\n  <svg viewBox=\"0 0 760 400\" role=\"img\" aria-labelledby=\"bp-fig1-title bp-fig1-desc\" xmlns=\"http:\/\/www.w3.org\/2000\/svg\">\n    <title id=\"bp-fig1-title\">Foundational Figure 1: the universal chain of pain production<\/title>\n    <desc id=\"bp-fig1-desc\">Nine-step chain arranged in three horizontal rows: stress, tissue, tissue adaptive capacity, then nociceptors, transmission via the spinal cord, brain integration, then pain, behavior, adaptation \u2014 with a feedback loop from adaptation back to tissue adaptive capacity.<\/desc>\n    <defs>\n      <marker id=\"arrowh1\" markerWidth=\"9\" markerHeight=\"9\" refX=\"6\" refY=\"3\" orient=\"auto\">\n        <path d=\"M0,0 L6,3 L0,6 Z\" fill=\"#185FA5\"\/>\n      <\/marker>\n      <marker id=\"arrowh2\" markerWidth=\"9\" markerHeight=\"9\" refX=\"6\" refY=\"3\" orient=\"auto\">\n        <path d=\"M0,0 L6,3 L0,6 Z\" fill=\"#2a9d5c\"\/>\n      <\/marker>\n    <\/defs>\n    <g font-family=\"Arial, sans-serif\">\n      <!-- Row 1: 1 \u2192 2 \u2192 3 -->\n      <rect x=\"20\" y=\"20\" width=\"200\" height=\"66\" rx=\"10\" fill=\"#eaf3fb\" stroke=\"#185FA5\"\/>\n      <text x=\"120\" y=\"58\" text-anchor=\"middle\" font-size=\"14\" font-weight=\"700\" fill=\"#0e2a47\">1. Stress<\/text>\n      <line x1=\"220\" y1=\"53\" x2=\"248\" y2=\"53\" stroke=\"#185FA5\" stroke-width=\"2\" marker-end=\"url(#arrowh1)\"\/>\n\n      <rect x=\"250\" y=\"20\" width=\"200\" height=\"66\" rx=\"10\" fill=\"#eaf3fb\" stroke=\"#185FA5\"\/>\n      <text x=\"350\" y=\"58\" text-anchor=\"middle\" font-size=\"14\" font-weight=\"700\" fill=\"#0e2a47\">2. Tissue<\/text>\n      <line x1=\"450\" y1=\"53\" x2=\"478\" y2=\"53\" stroke=\"#185FA5\" stroke-width=\"2\" marker-end=\"url(#arrowh1)\"\/>\n\n      <rect x=\"480\" y=\"20\" width=\"200\" height=\"66\" rx=\"10\" fill=\"#f0f8ff\" stroke=\"#185FA5\"\/>\n      <text x=\"580\" y=\"49\" text-anchor=\"middle\" font-size=\"12.5\" font-weight=\"700\" fill=\"#0e2a47\">3. Tissue adaptive<\/text>\n      <text x=\"580\" y=\"66\" text-anchor=\"middle\" font-size=\"12.5\" font-weight=\"700\" fill=\"#0e2a47\">capacity<\/text>\n      <line x1=\"580\" y1=\"86\" x2=\"580\" y2=\"114\" stroke=\"#185FA5\" stroke-width=\"2\" marker-end=\"url(#arrowh1)\"\/>\n\n      <!-- Row 2: 4 \u2190 5 \u2190 6 (runs back from right to left) -->\n      <rect x=\"480\" y=\"116\" width=\"200\" height=\"66\" rx=\"10\" fill=\"#eaf3fb\" stroke=\"#185FA5\"\/>\n      <text x=\"580\" y=\"154\" text-anchor=\"middle\" font-size=\"14\" font-weight=\"700\" fill=\"#0e2a47\">4. Nociceptors<\/text>\n      <line x1=\"480\" y1=\"149\" x2=\"452\" y2=\"149\" stroke=\"#185FA5\" stroke-width=\"2\" marker-end=\"url(#arrowh1)\"\/>\n\n      <rect x=\"250\" y=\"116\" width=\"200\" height=\"66\" rx=\"10\" fill=\"#eaf3fb\" stroke=\"#185FA5\"\/>\n      <text x=\"350\" y=\"146\" text-anchor=\"middle\" font-size=\"12.5\" font-weight=\"700\" fill=\"#0e2a47\">5. Transmission<\/text>\n      <text x=\"350\" y=\"162\" text-anchor=\"middle\" font-size=\"10.5\" fill=\"#5a6b7d\">(spinal cord)<\/text>\n      <line x1=\"250\" y1=\"149\" x2=\"222\" y2=\"149\" stroke=\"#185FA5\" stroke-width=\"2\" marker-end=\"url(#arrowh1)\"\/>\n\n      <rect x=\"20\" y=\"116\" width=\"200\" height=\"66\" rx=\"10\" fill=\"#eaf3fb\" stroke=\"#185FA5\"\/>\n      <text x=\"120\" y=\"154\" text-anchor=\"middle\" font-size=\"13\" font-weight=\"700\" fill=\"#0e2a47\">6. Brain integration<\/text>\n      <line x1=\"120\" y1=\"182\" x2=\"120\" y2=\"210\" stroke=\"#c0392b\" stroke-width=\"2\" marker-end=\"url(#arrowh1)\"\/>\n\n      <!-- Row 3: 7 \u2192 8 \u2192 9 -->\n      <rect x=\"20\" y=\"212\" width=\"200\" height=\"66\" rx=\"10\" fill=\"#fdecea\" stroke=\"#c0392b\"\/>\n      <text x=\"120\" y=\"252\" text-anchor=\"middle\" font-size=\"15\" font-weight=\"700\" fill=\"#c0392b\">7. Pain<\/text>\n      <line x1=\"220\" y1=\"245\" x2=\"248\" y2=\"245\" stroke=\"#185FA5\" stroke-width=\"2\" marker-end=\"url(#arrowh1)\"\/>\n\n      <rect x=\"250\" y=\"212\" width=\"200\" height=\"66\" rx=\"10\" fill=\"#eaf3fb\" stroke=\"#185FA5\"\/>\n      <text x=\"350\" y=\"252\" text-anchor=\"middle\" font-size=\"14\" font-weight=\"700\" fill=\"#0e2a47\">8. Behavior<\/text>\n      <line x1=\"450\" y1=\"245\" x2=\"478\" y2=\"245\" stroke=\"#2a9d5c\" stroke-width=\"2\" marker-end=\"url(#arrowh2)\"\/>\n\n      <rect x=\"480\" y=\"212\" width=\"200\" height=\"66\" rx=\"10\" fill=\"#eefaf1\" stroke=\"#2a9d5c\"\/>\n      <text x=\"580\" y=\"252\" text-anchor=\"middle\" font-size=\"14\" font-weight=\"700\" fill=\"#1f6b41\">9. Adaptation<\/text>\n\n      <!-- Feedback loop: 9 \u2192 3, along the right margin -->\n      <path d=\"M685,245 C 735,245 735,53 685,53\" fill=\"none\" stroke=\"#2a9d5c\" stroke-width=\"2\" stroke-dasharray=\"6 5\" marker-end=\"url(#arrowh2)\"\/>\n      <text x=\"748\" y=\"150\" font-size=\"10\" fill=\"#1f6b41\" transform=\"rotate(90 748 150)\" text-anchor=\"middle\">feedback on adaptive capacity<\/text>\n    <\/g>\n  <\/svg>\n  <figcaption>\n    <strong>Foundational Figure 1 \u2014 The universal chain of pain production.<\/strong> Pain\n    is never the direct and automatic consequence of a stress. It is the result of a chain that passes through\n    the adaptive capacity of the tissue involved and the activation of specialized receptors. This chain continues with nerve transmission and\n    brain integration. It then extends into a behavior \u2014 rest, avoidance, change of position \u2014 which in turn\n    modulates the tissue\u2019s adaptive capacity. It is this loop that explains why pain can evolve,\n    subside, or persist over time. This diagram is the summary representation of the biomechanical model.\n    All pages of this Knowledge Base that explain a pain mechanism refer directly back to it on this page.\n    They do so in the form \u201csee Figure 1 of the article \u2018Why Do I Hurt?\u2019,\u201d rather than reproducing it.\n  <\/figcaption>\n<\/figure>\n\n<!-- DURATION -->\n<h2 id=\"pourquoi-la-duree-change-tout\">Why duration changes everything<\/h2>\n<p>\n  Time is a variable just as important as the intensity of the stress itself. The same stress, if very brief, can\n  be perfectly well tolerated by a tissue. Repeated or sustained for several tens of\n  minutes, however, that same stress can gradually exceed its <strong>tissue adaptive capacity<\/strong>. This principle explains\n  why a sitting position that is comfortable at first can become painful after a certain time. Yet no\n  new event has occurred in the meantime: it is not the stress that has changed; it is the duration over which it is applied that\n  has ended up exceeding what the tissue could absorb.\n<\/p>\n<p>\n  <strong>Frequency of repetition<\/strong> is a third essential variable, on a par with intensity and\n  duration. A moderate stress, repeated hundreds of times a day, can produce the same consequences as a\n  much more intense but one-off stress. In that case, the tissue no longer has the time it needs to recover between two\n  loading episodes.\n<\/p>\n\n<!-- DISSOCIATION -->\n<h2 id=\"une-dissociation-essentielle-ou-j-ai-mal-n-est-pas-toujours-la-ou-ca-vient\">An essential dissociation: where it hurts is not always where it comes from<\/h2>\n<p>\n  This chain has a direct consequence, and it is probably the most counterintuitive idea in this article. The brain\n  generally localizes pain at the <strong>sensory nerve endings<\/strong> that transmitted the\n  signal. This is not necessarily where the structure that actually triggered the signal is located. Irritation occurring at one point\n  along a nerve\u2019s course can therefore be felt farther away, across all or part of its distribution territory.\n<\/p>\n<p>\n  This is not a matter of adding a component to the IASP definition, which remains the reference. Rather, it is a complementary\n  interpretive principle specific to this biomechanical model. It can be called a principle of\n  <strong>anatomoclinical dissociation<\/strong> between the site where the stress originates and the site where the pain\n  is perceived.\n<\/p>\n<p>\n  The origin of the signal can also lie directly along the course of the nerve itself \u2014 compression, an adhesion limiting its\n  gliding, prolonged irritation. When this is the case, rather than in a peripheral tissue that the nerve supplies, this is referred to as <strong>neuropathic\n  pain<\/strong>. It stems from damage to or a disturbance of the somatosensory nervous system, and not\n  from the simple activation of nociceptors by tissue stress.\n<\/p>\n\n<h3>Illustration: the pudendal nerve and Alcock\u2019s canal<\/h3>\n<p>\n  The example of pudendal neuralgia is particularly instructive. As it exits Alcock\u2019s canal, the pudendal nerve divides\n  into three branches. The first runs toward the clitoris or penis. The second in turn subdivides toward\n  the urethra on the one hand, and the labia or scrotum on the other. Finally, the third runs toward the anal canal.\n<\/p>\n<p>\n  The pain is perceived at these nerve endings, across all three territories or partially in one of them.\n  The origin of the problem, however, most often lies much farther upstream, precisely at Alcock\u2019s canal. It may be\n  compression of the nerve, fibrosis, or an adhesion that blocks its normal gliding. In summary:\n<\/p>\n<p style=\"text-align:center; font-weight:600; color:#0e2a47; background:#f4f8fb; border-radius:8px; padding:14px 18px;\">\n  Origin (Alcock\u2019s canal) \u2192 Transmission \u2192 Perception (anus \u00b7 vulva or penis \u00b7 urethra)\n<\/p>\n\n<figure class=\"bp-figure\">\n  <img decoding=\"async\"\n    src=\"https:\/\/blueportance.com\/wp-content\/uploads\/IMG_NP_Terminal-branches_Pudendal-nerve.jpg\"\n    alt=\"The terminal trident of the pudendal nerve: dorsal nerve (external genitalia), inferior rectal nerve (anal canal), deep perineal nerve and superficial perineal nerve (urogenital triangle, urethral sphincter, labia or scrotum), all branches arising from the same trunk at Alcock\u2019s canal\"\n    loading=\"lazy\"\n  \/>\n  <figcaption>\n    <strong>Figure 2 \u2014 Dissociation between site of origin and site of perception in pudendal neuralgia.<\/strong> The origin of the\n    problem (compression or an adhesion limiting nerve gliding) lies at Alcock\u2019s canal. The pain, however,\n    is perceived farther away, in one or more of the territories supplied by the terminal branches of the pudendal nerve \u2014 the dorsal\n    nerve, the inferior rectal nerve, and the deep and superficial perineal nerves.\n  <\/figcaption>\n<\/figure>\n\n<blockquote>\n  The brain does not always localize pain at the structure responsible for it. It localizes it at the\n  nerve endings that signaled it.\n<\/blockquote>\n\n<!-- NO APPARENT CAUSE -->\n<h2 id=\"puis-je-avoir-mal-sans-cause-apparente\">Can I be in pain without an apparent cause?<\/h2>\n<p>\n  Yes. But that does not mean the pain is imaginary. Several situations, which are not mutually exclusive,\n  can explain it:\n<\/p>\n\n<div class=\"bp-recognize\">\n  <h3>Four common situations<\/h3>\n  <ul>\n    <li><strong>The mechanical cause is very subtle<\/strong> \u2014 an adhesion, micro-instability, or muscle hypertonia cannot be seen with the naked eye and may go unnoticed during a standard examination.<\/li>\n    <li><strong>The cause is distant from the site where pain is felt<\/strong> \u2014 as in the example of Alcock\u2019s canal, where origin and perception do not coincide.<\/li>\n    <li><strong>The tissues have become hypersensitive<\/strong> \u2014 after prolonged irritation, some nerve structures can become more reactive. A slight load is then enough to trigger pain that initially would not have appeared.<\/li>\n    <li><strong>The test results are normal<\/strong> \u2014 MRI and CT scans show anatomical structures, but they do not always show how those structures behave functionally. A loss of tissue gliding, hypertonia, an adhesion, an instability that only appears under load, or an intermittent phenomenon that depends on posture or movement can therefore remain invisible.<\/li>\n  <\/ul>\n<\/div>\n\n<!-- TISSUE ADAPTIVE CAPACITY (III.3) -->\n<figure class=\"bp-figure\">\n  <img decoding=\"async\"\n    src=\"https:\/\/blueportance.com\/wp-content\/uploads\/III.3.Tissue-adaptability-the-key-factor.png\"\n    alt=\"Diagram illustrating the relationship between mechanical stress and a tissue\u2019s adaptive capacity.\"\n    loading=\"lazy\"\n  \/>\n  <figcaption>\n    <strong>Figure 3 \u2014 Tissue adaptive capacity<\/strong> (figure shared with the chapter \u201cNociceptive Pain\u201d). A stress challenges the\n    tissue\u2019s adaptive capacity. If that capacity is sufficient, the load can be tolerated, distributed, or compensated for, and the\n    response remains normal. If it is exceeded, nociceptors can be activated; if the signal persists beyond the initial stress,\n    sensitization may set in and the pain can become chronic. It is this branching point, more than the stress itself, that\n    helps determine whether pain remains a one-off episode or becomes long-lasting.\n  <\/figcaption>\n<\/figure>\n\n<div class=\"bp-definition\">\n  <p><strong>This article answers the question:<\/strong> why does pain appear?<\/p>\n<\/div>\n\n<!-- TRANSITION TO CHRONIC PAIN -->\n<h2 id=\"pourquoi-certaines-douleurs-deviennent-elles-chroniques\">Why does some pain become chronic?<\/h2>\n<p>\n  In some situations, the tissue that was initially loaded partially recovers, while the nervous system remains more\n  reactive. This is called <strong>sensitization<\/strong>, which can be <strong>peripheral<\/strong> (at the level of the\n  tissues) or <strong>central<\/strong> (at the level of the nervous system itself).\n<\/p>\n<p>\n  In some cases, a <strong>nociplastic<\/strong> component can also emerge. This is pain related to\n  altered processing of pain information. No tissue damage or involvement of the\n  somatosensory system is then sufficient to explain it <em>(Kosek et al., 2021)<\/em>. This mechanism mainly concerns\n  certain chronic pain conditions that have persisted for several months; it generally does not explain the initial onset of\n  mechanical sitting-related pain.\n<\/p>\n\n<h2 id=\"ce-que-cela-ne-veut-pas-dire\">What this does not mean<\/h2>\n<ul class=\"bp-errors\">\n  <li>Pain without a visible lesion is not pain that is \u201call in your head.\u201d<\/li>\n  <li>A normal test result does not mean that no mechanism explains it.<\/li>\n  <li>Pain felt far from its actual origin is not a perception error to be corrected, but information to be interpreted correctly.<\/li>\n  <li>Chronic or sensitized pain is not exaggerated pain: it is an alarm system whose settings have changed.<\/li>\n<\/ul>\n\n<p class=\"bp-founding-phrase\">\n  Pain is a message. Understanding that message is often more important than trying to silence it.<br>\n  <span>\u2014 Blue Portance biomechanical model<\/span>\n<\/p>\n\n<div class=\"bp-takeaway\">\n  <h2 id=\"a-retenir\">Key takeaways<\/h2>\n  <ul>\n    <li>Pain is an experience constructed by the nervous system \u2014 constructed does not mean imaginary.<\/li>\n    <li>It arises when a stress exceeds the adaptive capacity of a tissue: ligament, enthesis, muscle, fascia, or nerve, and rarely the bone itself.<\/li>\n    <li>The duration of a stress matters as much as its intensity.<\/li>\n    <li>The site where pain is felt is not always the site where the problem lies.<\/li>\n    <li>Pain without an apparent cause is not pain without a cause \u2014 and chronic pain is not exaggerated pain.<\/li>\n  <\/ul>\n<\/div>\n\n<!-- FURTHER READING -->\n<div class=\"bp-further\">\n  <h2 id=\"pour-aller-plus-loin\">Further reading<\/h2>\n  <ul>\n    <li><a href=\"https:\/\/blueportance.com\/en\/2026\/02\/09\/coccygodynia-pain-sitting\/\">Coccygodynia: Why Does Sitting Hurt So Much?<\/a><\/li>\n    <li><a href=\"https:\/\/blueportance.com\/en\/2026\/01\/11\/pudendal-neuralgia-sitting-pain\/\">Pudendal Neuralgia: Why Can a Simple Sitting Position Become an Ordeal?<\/a><\/li>\n    <li><a href=\"https:\/\/blueportance.com\/en\/knowledge-base\/expert-guides\/sitting-related-pain\/coccydynia\/\">Coccydynia (tailbone pain): the Expert Guide<\/a><\/li>\n    <li><a href=\"https:\/\/blueportance.com\/en\/2026\/01\/07\/pelvic-mobility-micro-movements\/\">Why Micro-Movement Matters More Than Moving a Lot<\/a><\/li>\n    <li><a href=\"https:\/\/blueportance.com\/en\/knowledge-base\/expert-guides\/understanding-pain\/\">Back to the Understanding Pain guide<\/a><\/li>\n    <li><a href=\"https:\/\/blueportance.com\/en\/knowledge-base\/\">Explore the Expert Guides<\/a><\/li>\n  <\/ul>\n<\/div>\n\n<!-- FAQ -->\n<section class=\"bp-faq\">\n  <h2 id=\"questions-frequentes-associees\">Related frequently asked questions<\/h2>\n  <details>\n    <summary>Can I be in pain without an apparent cause?<\/summary>\n    <div class=\"faq-content\">Yes, and that does not mean the pain is imaginary. The cause may be mechanically subtle (adhesion, micro-instability, hypertonia), distant from the site where pain is felt, or maintained by sensitization of the nervous system, which lowers the triggering threshold.<\/div>\n  <\/details>\n  <details>\n    <summary>Why can pain be felt in a location different from its origin?<\/summary>\n    <div class=\"faq-content\">Because the brain localizes pain at the sensory nerve endings, not necessarily at the structure that triggered the signal. Irritation at one point along a nerve\u2019s course can be felt farther away, across its distribution territory.<\/div>\n  <\/details>\n  <details>\n    <summary>Does a normal imaging test rule out a real cause for the pain?<\/summary>\n    <div class=\"faq-content\">No. MRI and CT scans show anatomical structures, but not always how they behave functionally. A loss of tissue gliding, muscle hypertonia, an adhesion, or an instability that only appears under load can therefore remain invisible on these tests.<\/div>\n  <\/details>\n  <details>\n    <summary>What is the difference between pain and suffering?<\/summary>\n    <div class=\"faq-content\">Pain is a biological signal. Suffering corresponds to what this signal produces in the person\u2019s life: worry, limitation of activities, fatigue, isolation. Both are real, but they do not arise from exactly the same mechanisms.<\/div>\n  <\/details>\n<\/section>\n\n<!-- CTA -->\n<div class=\"bp-cta\">\n  <h2 id=\"vous-reconnaissez-votre-situation\">Do you recognize your situation?<\/h2>\n  <p>Understanding the mechanism behind your pain is the first step toward analyzing it correctly.<\/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 aims to explain general pain mechanisms. It does not constitute a\n  medical diagnosis or a prescription, and it does not replace the advice of a healthcare professional.\n<\/p>\n\n<div class=\"bp-references\">\n  <h2 id=\"references-scientifiques\">Scientific references<\/h2>\n  <ol>\n    <li>Raja SN, Carr DB, Cohen M, et al. <em>The revised International Association for the Study of Pain definition of pain: concepts, challenges and compromises.<\/em> Pain. 2020;161(9):1976\u20131982.<\/li>\n    <li>International Association for the Study of Pain (IASP). <em>IASP Terminology \u2014 Pain Definition.<\/em> 2020.<\/li>\n    <li>Kosek E, Cohen M, Baron R, et al. <em>Chronic nociplastic pain affecting the musculoskeletal system: clinical criteria and grading system.<\/em> Pain. 2021;162(11):2629\u20132634.<\/li>\n<\/ol>\n  <h3>Further reading<\/h3>\n  <ul>\n    <li>Basbaum AI, Bautista DM, Scherrer G, Julius D. <em>Cellular and Molecular Mechanisms of Pain.<\/em> Cell. 2009;139(2):267\u2013284.<\/li>\n    <li>Treede RD. <em>The role of quantitative sensory testing in the prediction of chronic pain.<\/em> Pain. 2019;160 Suppl 1:S66\u2013S69. doi:10.1097\/j.pain.0000000000001544.<\/li>\n  <\/ul>\n<\/div>\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\n","protected":false},"excerpt":{"rendered":"<p>Blue Portance \u2192 Knowledge Base \u2192 Understanding Pain \u2192 Why Do I Hurt? Blue Portance Expert Guides Understanding Pain The biological, mechanical, and neurophysiological mechanisms that explain the onset and persistence of sitting-related pain. This article is part of the \u201cUnderstanding Pain\u201d Expert Guide. Foundational article \u2014 Blue Portance Knowledge Base Why Do I Hurt? [&#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":"Why Do I Hurt? 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