{"id":8041,"date":"2026-07-17T13:24:01","date_gmt":"2026-07-17T11:24:01","guid":{"rendered":"https:\/\/blueportance.com\/knowledge-base\/expert-guides\/understanding-pain\/neuropathic-pain\/"},"modified":"2026-10-25T22:43:25","modified_gmt":"2026-10-25T21:43:25","slug":"neuropathic-pain","status":"publish","type":"page","link":"https:\/\/blueportance.com\/en\/knowledge-base\/expert-guides\/understanding-pain\/neuropathic-pain\/","title":{"rendered":"KB 3_Expert Guide_01_Understanding Pain_05_Neuropathic Pain"},"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-dossier-subtitle{color:#3a6d8a;font-size:.94rem;font-style:italic;line-height:1.6;margin:10px 0 20px}\n    .bp-bdc-dossier-link{margin:0 0 26px;font-size:.9rem;color:#3a6d8a}\n    .bp-bdc-dossier-link a{color:#2a7fba;font-weight:600;text-decoration:none}\n    .bp-bdc-epistemic{margin:0 0 24px;padding:15px 18px;border-left:4px solid #d39b22;border-radius:6px;background:#fff8e1;color:#5a4a00;font-size:.9rem}\n    .bp-inline-ref{white-space:nowrap;font-size:.88em;color:#5f6f7d}\n    @media(max-width:640px){body{padding:16px}h1{font-size:1.5rem}table{display:block;overflow-x:auto}}\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<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<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 Neuropathic 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\">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>When Does Nerve Damage Become Neuropathic Pain?<\/h1>\n\n<div class=\"bp-bdc-epistemic\">\n  <strong>Epistemic note<\/strong> \u2014 This article distinguishes the international definition of neuropathic pain, the biological mechanisms established after a lesion or disease of the somatosensory system, and the biomechanical reading proposed by Blue Portance. Pain located along the course of a nerve, a burning sensation, or radiating pain is not enough to establish neuropathic pain. The diagnosis rests on a compatible history, a neuroanatomically plausible distribution, consistent sensory signs and, when possible, demonstration of the lesion or disease involved. Data on treatments and surgical outcomes describe general trends and cannot predict how an individual case will evolve.\n<\/div>\n\n<section class=\"bp-summary\">\n  <p>\n    <strong>Summary<\/strong> \u2014 Neuropathic pain is caused by a lesion or disease of the somatosensory nervous system. It is therefore not simply pain located near a nerve. Indeed, after compression, trauma, surgery, or a neurological disease, the nerve and the circuits that process its information can remain altered over the long term. A mechanical stress may thus have disappeared while the myelin, the axons, or the sensory pathways have not yet recovered. The pain may then persist, fluctuate, or become partly independent of the initial cause. This situation is also particularly important after nerve decompression: removing the entrapment does not mean that all of its biological consequences disappear immediately.\n  <\/p>\n<\/section>\n\n<nav class=\"bp-bdc-toc\" aria-label=\"Contents\">\n  <h2>Contents<\/h2>\n  <ul>\n      <li><a href=\"#pourquoi-cet-article-est-il-important\">Why does this article matter?<\/a><\/li>\n      <li><a href=\"#1-quappelle-t-on-reellement-une-douleur-neuropathique\">1. What exactly is neuropathic pain?<\/a><\/li>\n      <li><a href=\"#2-comment-etablit-on-quune-douleur-est-neuropathique\">2. How is pain established as neuropathic?<\/a><\/li>\n      <li><a href=\"#3-que-se-passe-t-il-apres-une-lesion-nerveuse\">3. What happens after a nerve injury?<\/a><\/li>\n      <li><a href=\"#4-pourquoi-la-douleur-peut-elle-persister-apres-la-suppression-de-la-cause-initiale\">4. Why can pain persist after the initial cause has been removed?<\/a><\/li>\n      <li><a href=\"#5-le-cas-particulier-de-la-decompression-du-nerf-pudendal\">5. The special case of pudendal nerve decompression<\/a><\/li>\n      <li><a href=\"#6-quelles-sont-les-principales-causes-de-douleur-neuropathique\">6. What are the main causes of neuropathic pain?<\/a><\/li>\n      <li><a href=\"#7-comment-comprendre-les-symptomes\">7. How should the symptoms be understood?<\/a><\/li>\n      <li><a href=\"#8-comment-la-douleur-neuropathique-est-elle-prise-en-charge\">8. How is neuropathic pain managed?<\/a><\/li>\n      <li><a href=\"#lecture-proposee-par-le-modele-blue-portance\">Reading proposed by the Blue Portance model<\/a><\/li>\n      <li><a href=\"#9-ce-que-lassise-peut-et-ne-peut-pas-modifier\">9. What sitting can \u2014 and cannot \u2014 change<\/a><\/li>\n      <li><a href=\"#10-douleur-neuropathique-et-douleur-nociplastique-ou-se-situe-la-frontiere\">10. Neuropathic pain and nociplastic pain: where is the boundary?<\/a><\/li>\n      <li><a href=\"#11-controverses-et-limites-des-connaissances-actuelles\">11. Controversies and limits of current knowledge<\/a><\/li>\n      <li><a href=\"#12-consequences-pratiques-pour-comprendre-une-situation\">12. 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 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-il-important\">Why does this article matter?<\/h2>\n\n<p>\n  The previous article explained how compression, tension, or a loss of gliding could load a nerve, disrupt its microcirculation and, in some situations, cause true somatosensory damage. It also showed that a nerve can be painful without necessarily being injured: its sheaths, its blood vessels, and the neighboring tissues can produce nociceptive activity.\n<\/p>\n\n<p>\n  Another question therefore arises: what happens once a nerve lesion is established? Why do some people continue to suffer even though the compression has been removed, the scar has healed, or imaging no longer shows any obvious conflict? And why does a procedure intended to free a nerve not always make the pain disappear immediately?\n<\/p>\n\n<p>\n  These situations do not necessarily mean that the procedure performed was useless or that the pain is \u201cpsychological.\u201d Rather, they are a reminder that a nerve is not a cable that can be put back into service instantly as soon as the pressure is removed. It is a living, vascularized, and organized tissue whose recovery depends on the nature of the damage, its duration, and the biological background.\n<\/p>\n\n<div class=\"bp-figure\">\n  <img decoding=\"async\" src=\"https:\/\/blueportance.com\/wp-content\/uploads\/V.1.Not-all-nerve-pain-is-neuropathic.png\" alt=\"Comparison of nerve sheath pain, neuropathic pain and referred pain.\" loading=\"lazy\">\n<\/div>\n<p class=\"bp-figure-caption\">\n  <strong>Figure 1 \u2014 Not all nerve pain is neuropathic.<\/strong> Pain located near a nerve may arise from the nerve sheaths, from true damage to the somatosensory system, or be referred from another anatomical structure. The distinction rests on the mechanism, the clinical features, and the pain distribution.\n<\/p>\n\n<blockquote>\n  Removing a mechanical stress can eliminate the cause that sustains the damage. It does not guarantee that nerve function, conduction, and the sensory processing circuits will immediately return to their previous state.\n<\/blockquote>\n\n<p>\n  A nerve can therefore suffer without being injured. But is that suffering enough to speak of neuropathic pain? No. We first need to clarify what this concept covers.\n<\/p>\n\n<h2 id=\"1-quappelle-t-on-reellement-une-douleur-neuropathique\">1. What exactly is neuropathic pain?<\/h2>\n\n<div class=\"bp-definition\">\n  <strong class=\"bp-def-source\">Reference 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  The somatosensory system receives and processes information related to touch, pressure, temperature, body position, and potentially harmful stimuli. Damage may therefore involve a peripheral nerve, a nerve root, a plexus, the spinal cord, the brainstem, the thalamus, or other brain structures involved in sensory processing <span class=\"bp-inline-ref\">(Colloca et&nbsp;al., 2017; Finnerup et&nbsp;al., 2016)<\/span>.\n<\/p>\n\n<div class=\"bp-figure\">\n  <img decoding=\"async\" src=\"https:\/\/blueportance.com\/wp-content\/uploads\/V.2.The-somatosensory-system-an-impairment-at-any-level-can-lead-to-neuropathic-pain.png\" alt=\"Somatosensory pathway from peripheral receptors to the cortex showing possible sites of neuropathic pain.\" loading=\"lazy\">\n<\/div>\n<p class=\"bp-figure-caption\">\n  <strong>Figure 2 \u2014 The somatosensory system and neuropathic pain.<\/strong> Neuropathic pain can result from a lesion or disease affecting any level of the somatosensory system, from the peripheral nerve fibers to the central structures.\n<\/p>\n\n<p>\n  Neuropathic pain is therefore defined by its <strong>causal mechanism<\/strong>, not by its intensity or by an adjective used to describe it. Burning, electric, or radiating pain can guide the examination, but these qualities do not prove that a somatosensory lesion exists. Likewise, nerve damage may cause little pain and show up mainly as numbness, loss of sensation, weakness, or clumsiness <span class=\"bp-inline-ref\">(Finnerup et&nbsp;al., 2016; Truini et&nbsp;al., 2023)<\/span>.\n<\/p>\n\n<h3>Nerve trunk pain and neuropathic pain are not synonymous<\/h3>\n\n<p>\n  When local pressure loads the epineurium, the <em>nervi nervorum<\/em>, the blood vessels, or a neighboring interface, nociceptive pain can occur without demonstrated injury to the sensory fibers. Conversely, when a lesion or disease of the somatosensory system is established, the pain arises from a neuropathic mechanism <span class=\"bp-inline-ref\">(Bove, 2008; Finnerup et&nbsp;al., 2016)<\/span>.\n<\/p>\n\n<table aria-label=\"Difference between pain near a nerve and neuropathic pain\">\n  <thead>\n    <tr>\n      <th>Situation<\/th>\n      <th>Possible mechanism<\/th>\n      <th>What allows a conclusion<\/th>\n    <\/tr>\n  <\/thead>\n  <tbody>\n    <tr>\n      <td>Pain localized near a nerve<\/td>\n      <td>Loading of the sheaths, blood vessels, or neighboring tissues<\/td>\n      <td>Anatomical proximity is not enough to demonstrate a neuropathy<\/td>\n    <\/tr>\n    <tr>\n      <td>Burning, electric shocks, tingling<\/td>\n      <td>May accompany nerve damage, but are not specific<\/td>\n      <td>They are clues to be integrated with the history and the examination<\/td>\n    <\/tr>\n    <tr>\n      <td>Neuropathic pain<\/td>\n      <td>Lesion or disease of the somatosensory system<\/td>\n      <td>Plausible distribution, consistent sensory signs, and evidence of the damage when possible<\/td>\n    <\/tr>\n  <\/tbody>\n<\/table>\n\n<p>\n  This definition, however, is not enough to make a diagnosis. We still need to know how to establish it in practice.\n<\/p>\n\n<h2 id=\"2-comment-etablit-on-quune-douleur-est-neuropathique\">2. How is pain established as neuropathic?<\/h2>\n\n<p>\n  The diagnosis does not rest on a single word or on a questionnaire taken in isolation. Rather, it combines the clinical history, the distribution of symptoms, the neurological examination and, depending on the situation, diagnostic testing. In particular, the grading system proposed by the NeuPSIG group distinguishes several levels of certainty <span class=\"bp-inline-ref\">(Finnerup et&nbsp;al., 2016; Truini et&nbsp;al., 2023)<\/span>.\n<\/p>\n\n<div class=\"bp-figure\">\n  <img decoding=\"async\" src=\"https:\/\/blueportance.com\/wp-content\/uploads\/V.3.How-is-neuropathic-pain-diagnosed.png\" alt=\"Four-step clinical approach to diagnosing neuropathic pain with NeuPSIG levels of certainty.\" loading=\"lazy\">\n<\/div>\n<p class=\"bp-figure-caption\">\n  <strong>Figure 3 \u2014 How is neuropathic pain diagnosed?<\/strong> The diagnosis rests on the combination of a compatible clinical history, a consistent pain distribution, neurological signs and, when necessary, diagnostic testing.\n<\/p>\n\n<h3>A history compatible with a neurological lesion or disease<\/h3>\n\n<p>\n  The first question is causal: is there an event or a disease that could have damaged the somatosensory system? This may be trauma, surgery, prolonged compression, shingles (herpes zoster), diabetes, chemotherapy, radiculopathy, stroke, or a spinal cord injury.\n<\/p>\n\n<p>\n  Pain that appeared after an operation is not, however, enough to prove a nerve lesion. The scar, inflammation, muscles, ligaments, and mechanical interfaces can also produce pain. The history must therefore be consistent with the distribution and the signs observed.\n<\/p>\n\n<h3>A neuroanatomically plausible distribution<\/h3>\n\n<p>\n  The symptoms must be located in an area compatible with the nerve, the nerve root, or the central structure involved. In practice, this distribution is not always sharply delimited: territories overlap, the pain may extend beyond the area of deficit, and secondary changes can alter how it presents.\n<\/p>\n\n<p>\n  Nevertheless, diffuse pain with no neuroanatomical consistency cannot be classified as neuropathic solely on the basis of burning sensations or electric shocks.\n<\/p>\n\n<h3>Positive and negative sensory signs<\/h3>\n\n<p>\n  The examination looks for positive signs \u2014 allodynia, hyperalgesia, dysesthesias, paresthesias \u2014 and negative signs \u2014 reduced sensation to touch, pinprick, temperature, or vibration. Their location must be compatible with the structure presumed to be damaged <span class=\"bp-inline-ref\">(Finnerup et&nbsp;al., 2016; Truini et&nbsp;al., 2023)<\/span>.\n<\/p>\n\n<p>\n  Positive signs reflect abnormal excitability or sensory processing. Negative signs, for their part, indicate a loss of function. Moreover, the two frequently coexist: the same area can be both numb and painful.\n<\/p>\n\n<h3>Diagnostic testing<\/h3>\n\n<p>\n  Electrodiagnostic testing (electromyography and nerve conduction studies, EMG\/NCS) can reveal certain large-fiber neuropathies, conduction slowing, or axonal loss. It may, however, be normal in small-fiber damage or in some very focal lesions. Likewise, imaging can identify an anatomical cause, a central lesion, or a compression, but an abnormal image does not always prove that it explains the pain <span class=\"bp-inline-ref\">(Truini et&nbsp;al., 2023; Colloca et&nbsp;al., 2017)<\/span>.\n<\/p>\n\n<p>\n  Depending on the context, quantitative sensory testing, a skin biopsy, evoked potentials, or other investigations may be offered. No test, however, replaces the clinical integration of all the data.\n<\/p>\n\n<table aria-label=\"Grading of neuropathic pain\">\n  <thead>\n    <tr>\n      <th>Level of certainty<\/th>\n      <th>Expected elements<\/th>\n    <\/tr>\n  <\/thead>\n  <tbody>\n    <tr>\n      <td><strong>Possible<\/strong><\/td>\n      <td>History compatible with a neurological lesion or disease and a neuroanatomically plausible distribution.<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Probable<\/strong><\/td>\n      <td>The previous elements plus consistent sensory signs on examination.<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Definite<\/strong><\/td>\n      <td>The previous elements plus demonstration of the lesion or disease that could explain the pain.<\/td>\n    <\/tr>\n  <\/tbody>\n<\/table>\n\n<div class=\"bp-controversy\">\n  <h3>Diagnostic certainty is not absolute proof of causation<\/h3>\n  <p>\n    Even at the \u201cdefinite\u201d level, a lesion can coexist with other pain generators. A herniated disc, a neuropathy, or a nerve scar does not automatically explain all of the symptoms. The analysis must therefore look for associated mechanisms.\n  <\/p>\n<\/div>\n\n<p>\n  Diagnostic certainty, however, still says nothing about what will become of the nerve biologically. What actually happens in the tissues once the lesion is established?\n<\/p>\n\n<h2 id=\"3-que-se-passe-t-il-apres-une-lesion-nerveuse\">3. What happens after a nerve injury?<\/h2>\n\n<p>\n  A nerve lesion does not simply interrupt conduction. It triggers a series of biological responses in the axons, the myelin, the Schwann cells, the immune cells, the sensory ganglia, and the central circuits. In fact, the intensity of the pain does not directly reflect the extent of the lesion: minor damage can be very painful, while a severe neuropathy may mainly cause a loss of sensation <span class=\"bp-inline-ref\">(Campbell &amp; Meyer, 2006; Kocot-K\u0119pska et&nbsp;al., 2021)<\/span>.\n<\/p>\n\n<h3>Demyelination and altered conduction<\/h3>\n\n<p>\n  Myelin allows fast, organized conduction. When it is damaged, the signal can slow down, be blocked, or propagate unstably. Demyelinated areas can also become sensitive to mechanical changes or promote abnormal interactions between neighboring fibers <span class=\"bp-inline-ref\">(Mackinnon, 2002; Menorca et&nbsp;al., 2013)<\/span>.\n<\/p>\n\n<h3>Axonal damage and ectopic activity<\/h3>\n\n<p>\n  When an axon is injured, its membrane and the distribution of its ion channels change. As a result, spontaneous discharges can arise at the lesion site, in a neuroma, or in the sensory ganglion. The nervous system then receives messages that no longer faithfully reflect an actual peripheral stimulus <span class=\"bp-inline-ref\">(Campbell &amp; Meyer, 2006; Kocot-K\u0119pska et&nbsp;al., 2021)<\/span>.\n<\/p>\n\n<p>\n  In concrete terms, this activity can show up as spontaneous pain, paroxysmal discharges, paresthesias, or excessive sensitivity to touch. It can therefore persist even when the initial pressure has disappeared, because it now depends on the biological consequences of the damage.\n<\/p>\n\n<h3>Regeneration, sprouting, and neuroma<\/h3>\n\n<p>\n  After a lesion, peripheral axons may try to grow back. This regeneration is slow, however, and depends on the continuity of the sheaths, the distance to be covered, the blood supply, and the condition of the tissues. When the fibers do not find their way or run into scar tissue, a cluster of regenerating fibers can form: a neuroma <span class=\"bp-inline-ref\">(Menorca et&nbsp;al., 2013)<\/span>.\n<\/p>\n\n<p>\n  A neuroma is not always painful. When it is, however, it can be sensitive to pressure, movement, or stretching and produce spontaneous or provoked discharges.\n<\/p>\n\n<h3>Immune response and local sensitization<\/h3>\n\n<p>\n  Schwann cells, macrophages, and other immune cells take part in clearing debris and repairing the nerve. This response is essential, but it also releases mediators that can change the excitability of the remaining fibers. Prolonged neuroimmune inflammation can thus sustain the nerve&#8217;s sensitivity <span class=\"bp-inline-ref\">(Kocot-K\u0119pska et&nbsp;al., 2021)<\/span>.\n<\/p>\n\n<h3>Spinal and brain changes<\/h3>\n\n<p>\n  Repeated abnormal activity coming from an injured nerve can alter the neurons of the dorsal horn and the descending modulation systems. In concrete terms, receptive fields can expand, inhibitory mechanisms can weaken, and certain responses can become excessive <span class=\"bp-inline-ref\">(Latremoliere &amp; Woolf, 2009; Campbell &amp; Meyer, 2006)<\/span>.\n<\/p>\n\n<p>\n  These central changes are part of the pathophysiology of many chronic neuropathic pain conditions. They do not mean, however, that the peripheral lesion no longer exists or that the pain has automatically become nociplastic. In reality, peripheral and central mechanisms can coexist and sustain each other.\n<\/p>\n\n<div class=\"bp-figure\">\n  <img decoding=\"async\" src=\"https:\/\/blueportance.com\/wp-content\/uploads\/V.4.The-biological-evolution-of-a-nerve-after-a-lesion.png\" alt=\"Biological sequence from nerve injury to demyelination, axonal damage, ectopic activity and neuropathic pain.\" loading=\"lazy\">\n<\/div>\n<p class=\"bp-figure-caption\">\n  <strong>Figure 4 \u2014 What happens biologically to a nerve after a lesion.<\/strong> Depending on the severity of the damage and the quality of the repair, a nerve can return to normal function or progress to persistent neuropathic pain.\n<\/p>\n\n<p>\n  Once set in motion, these biological changes do not yet explain everything. They do, however, help us understand why pain can continue long after its initial cause has disappeared.\n<\/p>\n\n<h2 id=\"4-pourquoi-la-douleur-peut-elle-persister-apres-la-suppression-de-la-cause-initiale\">4. Why can pain persist after the initial cause has been removed?<\/h2>\n\n<p>\n  Decompression, removal of a herniated disc, recovery from shingles, or the healing of an injury can remove or reduce the initial factor. Yet the pain does not always disappear at the same pace. Several explanations are possible, and they can combine.\n<\/p>\n\n<h3>The nerve needs time to recover<\/h3>\n\n<p>\n  A transient microcirculatory disturbance can recover quickly. Demyelination takes longer. Axonal damage requires slow and sometimes incomplete regeneration. Recovery therefore depends on what was actually damaged before the stress was removed <span class=\"bp-inline-ref\">(Mackinnon, 2002; Menorca et&nbsp;al., 2013)<\/span>.\n<\/p>\n\n<p>\n  Pain that persists in the weeks or months following a procedure does not, on its own, show that the procedure has failed. It may reflect a recovery period, ongoing regeneration, or circuits that are still hyperexcitable.\n<\/p>\n\n<h3>The lesion may be partly irreversible<\/h3>\n\n<p>\n  If a large proportion of axons has been destroyed, if the compression lasted a long time, or if the biological background limits regeneration, recovery may remain incomplete. In that case, removing the cause prevents further deterioration without allowing a full return to the previous state.\n<\/p>\n\n<h3>Ectopic activity can persist<\/h3>\n\n<p>\n  Injured or regenerating fibers can continue to produce spontaneous discharges. As a result, the pain signal is no longer triggered solely by the initial pressure. It also comes from the abnormal electrical behavior of the altered nerve tissue <span class=\"bp-inline-ref\">(Campbell &amp; Meyer, 2006; Kocot-K\u0119pska et&nbsp;al., 2021)<\/span>.\n<\/p>\n\n<h3>The scar can create a new mechanical interface<\/h3>\n\n<p>\n  Surgery changes the tissue planes. Adhesions, fibrosis, or reduced gliding can therefore develop around the nerve. The area that was initially decompressed may be freed, while a new stress forms at the scar or at a neighboring interface <span class=\"bp-inline-ref\">(Schmid et&nbsp;al., 2020; Menorca et&nbsp;al., 2013)<\/span>.\n<\/p>\n\n<h3>Central circuits do not return to normal instantly<\/h3>\n\n<p>\n  When pain has lasted a long time, spinal neurons and brain modulation systems may have adapted to an abnormal flow of information. In practice, a reduction in the peripheral signal is therefore not always enough to immediately restore inhibition and the precision of sensory processing <span class=\"bp-inline-ref\">(Latremoliere &amp; Woolf, 2009; Colloca et&nbsp;al., 2017)<\/span>.\n<\/p>\n\n<h3>The pain may be mixed<\/h3>\n\n<p>\n  Neuropathic pain can coexist with scar, muscle, joint, fascial, or visceral pain. A procedure may then correct one component without eliminating the others. In pelvic pain in particular, this coexistence is especially common because of the density of the structures, interfaces, and sensory systems involved.\n<\/p>\n\n<div class=\"bp-recognize\">\n  <h3>Persistent pain after decompression may therefore reflect:<\/h3>\n  <ul>\n    <li>nerve recovery that is still in progress;<\/li>\n    <li>persistent demyelination or axonal damage;<\/li>\n    <li>spontaneous activity of injured or regenerating fibers;<\/li>\n    <li>a sensitive neuroma or scar;<\/li>\n    <li>a new loss of gliding around the nerve;<\/li>\n    <li>secondary central changes;<\/li>\n    <li>another associated source of pain;<\/li>\n    <li>an incomplete initial diagnosis or a different dominant mechanism.<\/li>\n  <\/ul>\n<\/div>\n\n<div class=\"bp-figure\">\n  <img decoding=\"async\" src=\"https:\/\/blueportance.com\/wp-content\/uploads\/V.5.Why-can-neuropathic-pain-persist-even-after-the-cause-has-disappeared.png\" alt=\"Diagram showing sufficient versus incomplete nerve recovery after removal of an initial mechanical cause.\" loading=\"lazy\">\n<\/div>\n<p class=\"bp-figure-caption\">\n  <strong>Figure 5 \u2014 Why can neuropathic pain persist even after the cause has disappeared?<\/strong> Once established, certain biological and neuroplastic changes can sustain the pain even when the initial lesion has disappeared.\n<\/p>\n\n<p>\n  This question of persistence takes on particular significance when surgery has specifically aimed to remove the stress. The pudendal nerve offers a telling example.\n<\/p>\n\n<h2 id=\"5-le-cas-particulier-de-la-decompression-du-nerf-pudendal\">5. The special case of pudendal nerve decompression<\/h2>\n\n<p>\n  The pudendal nerve passes through several anatomical interfaces that can limit its gliding or reduce the available space, particularly near the ischial spine and in the pudendal canal. In some people who meet specific clinical criteria, surgical decompression may be offered after conservative approaches have failed.\n<\/p>\n\n<p>\n  The goal of the procedure is mechanical: to free a presumed area of entrapment and restore a more favorable environment for the nerve. On its own, however, it cannot guarantee the immediate disappearance of all the biological consequences that built up before surgery. In practice, a recovery period therefore remains usual.\n<\/p>\n\n<h3>What surgery can correct<\/h3>\n\n<ul>\n  <li>an identified compression or anatomical conflict;<\/li>\n  <li>a local restriction of the available space;<\/li>\n  <li>part of the stress exerted by certain ligamentous or scar structures;<\/li>\n  <li>the mechanical conditions likely to sustain the damage.<\/li>\n<\/ul>\n\n<h3>What it does not automatically correct<\/h3>\n\n<ul>\n  <li>axonal loss that is already established;<\/li>\n  <li>extensive demyelination;<\/li>\n  <li>established ectopic activity;<\/li>\n  <li>the spinal and brain changes associated with chronic pain;<\/li>\n  <li>other sources of perineal or pelvic pain;<\/li>\n  <li>scar hypersensitivity or new adhesions;<\/li>\n  <li>an initial diagnosis that does not correspond to a true entrapment.<\/li>\n<\/ul>\n\n<p>\n  Published results for pudendal decompression techniques are heterogeneous. Some people improve markedly, others partially, late, or only slightly. Moreover, the available studies differ in their selection criteria, surgical techniques, follow-up durations, and outcome measures. Recent reviews still point to the lack of a solid consensus that would allow the effectiveness and risks for a given person to be predicted precisely <span class=\"bp-inline-ref\">(Mylle et&nbsp;al., 2024; Andiman et&nbsp;al., 2025)<\/span>.\n<\/p>\n\n<p>\n  More intense pain after a procedure should therefore prompt a reassessment, without automatically settling on a single explanation. It is necessary to distinguish expected postoperative pain, nerve recovery, a complication, a sensitive scar, a new stress, a persistent neuropathy, and other associated pain mechanisms.\n<\/p>\n\n<div class=\"bp-controversy\">\n  <h3>Can a technically successful operation be followed by persistent pain?<\/h3>\n  <p>\n    Yes. The anatomical success of a decompression and the clinical course do not always line up immediately. Surgery may have removed the entrapment before the nerve has recovered, or without the other pain components having disappeared. Conversely, persistent pain may also signal insufficient effectiveness, a complication, or an initial diagnosis that needs to be reconsidered. In short, only a clinical evaluation can tell these situations apart.\n  <\/p>\n<\/div>\n\n<p>\n  Beyond this particular case, a number of clinical situations can lead to a lesion of the somatosensory system.\n<\/p>\n\n<h2 id=\"6-quelles-sont-les-principales-causes-de-douleur-neuropathique\">6. What are the main causes of neuropathic pain?<\/h2>\n\n<table aria-label=\"Main causes of neuropathic pain\">\n  <thead>\n    <tr>\n      <th>Category<\/th>\n      <th>Examples<\/th>\n      <th>Possible type of damage<\/th>\n    <\/tr>\n  <\/thead>\n  <tbody>\n    <tr>\n      <td><strong>Compression or entrapment<\/strong><\/td>\n      <td>Carpal tunnel, ulnar neuropathy, certain radiculopathies, certain pudendal entrapments<\/td>\n      <td>Ischemia, focal demyelination, axonal damage<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Trauma or surgery<\/strong><\/td>\n      <td>Transection, severe stretch, iatrogenic injury, neuroma<\/td>\n      <td>Axonal interruption, disorganized regeneration, scarring<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Metabolic disease<\/strong><\/td>\n      <td>Diabetes, specific deficiency, kidney failure<\/td>\n      <td>Polyneuropathy, small- or large-fiber damage<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Infection<\/strong><\/td>\n      <td>Shingles, HIV, certain neurological infections<\/td>\n      <td>Ganglionic, radicular, or peripheral damage<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Toxicity<\/strong><\/td>\n      <td>Chemotherapy, certain medications or toxins<\/td>\n      <td>Diffuse axonal or small-fiber damage<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Inflammatory or autoimmune disease<\/strong><\/td>\n      <td>Inflammatory neuropathies, multiple sclerosis<\/td>\n      <td>Peripheral or central demyelination or axonal damage<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Central lesion<\/strong><\/td>\n      <td>Stroke, spinal cord injury, syringomyelia<\/td>\n      <td>Damage to the central somatosensory pathways<\/td>\n    <\/tr>\n  <\/tbody>\n<\/table>\n\n<p>\n  Whatever the cause, this damage translates in practice into a set of characteristic symptoms.\n<\/p>\n\n<h2 id=\"7-comment-comprendre-les-symptomes\">7. How should the symptoms be understood?<\/h2>\n\n<p>\n  Neuropathic pain often combines spontaneous and provoked symptoms. The combination varies with the structure injured, the type of fibers involved, and secondary changes.\n<\/p>\n\n<h3>Spontaneous symptoms<\/h3>\n\n<ul>\n  <li>continuous or fluctuating burning;<\/li>\n  <li>electric-shock sensations or brief shooting pains;<\/li>\n  <li>tingling, pins and needles, or current-like sensations;<\/li>\n  <li>deep, squeezing, or cold pain;<\/li>\n  <li>painful numbness.<\/li>\n<\/ul>\n\n<h3>Provoked symptoms<\/h3>\n\n<ul>\n  <li><strong>mechanical allodynia:<\/strong> pain from the rubbing of clothing or from contact that is normally not painful;<\/li>\n  <li><strong>hyperalgesia:<\/strong> an excessive response to a painful stimulus;<\/li>\n  <li><strong>pain with movement or tension:<\/strong> when the nerve or its interfaces remain mechanosensitive;<\/li>\n  <li><strong>pain with pressure:<\/strong> possible over a nerve trunk, a neuroma, or a scar.<\/li>\n<\/ul>\n\n<p>\n  None of these signs is sufficient on its own. Their value depends on their distribution, on whether they are associated with sensory deficits, and on the presence of a compatible lesion or disease.\n<\/p>\n\n<p>\n  Identifying these symptoms then naturally raises the question of management.\n<\/p>\n\n<h2 id=\"8-comment-la-douleur-neuropathique-est-elle-prise-en-charge\">8. How is neuropathic pain managed?<\/h2>\n\n<p>\n  Management depends on the cause, the location, how long the pain has been present, the associated deficits, and the other pain mechanisms. It is often multimodal, because treating only one aspect is not always enough.\n<\/p>\n\n<h3>Identifying and treating the cause when it is still active<\/h3>\n\n<p>\n  Persistent compression, metabolic disease, inflammation, infection, or toxicity should therefore be looked for and addressed. When the cause can be removed, the goal is to prevent the damage from continuing and to create the most favorable conditions for recovery.\n<\/p>\n\n<h3>Reducing the neuropathic pain itself<\/h3>\n\n<p>\n  Conventional pain relievers are often insufficient. Accordingly, treatments that act on nerve excitability or descending modulation may be offered by a physician depending on the type of neuropathy, contraindications, and tolerance. Recent recommendations confirm that average effectiveness remains modest and variable: the goal is often a meaningful reduction in pain and an improvement in function rather than complete elimination in every case <span class=\"bp-inline-ref\">(Finnerup et&nbsp;al., 2015; Soliman et&nbsp;al., 2025)<\/span>.\n<\/p>\n\n<h3>Preserving or restoring function<\/h3>\n\n<p>\n  Rehabilitation aims to limit deconditioning, preserve mobility, reduce avoidance behaviors, and gradually reintroduce activities compatible with the condition of the nerve. In particular, neural mobilization techniques are not forced stretching: they must respect sensitivity, deficits, and the postoperative context.\n<\/p>\n\n<h3>Taking sleep, activity, and psychological consequences into account<\/h3>\n\n<p>\n  Chronic pain disrupts sleep, attention, mood, and social activities. These consequences can in turn reduce recovery capacity and increase the overall load on the system. Addressing them does not mean that the pain is psychological; the aim is to limit the mechanisms that sustain it and to restore quality of life.\n<\/p>\n\n<h3>Interventional techniques and neuromodulation<\/h3>\n\n<p>\n  Finally, for some treatment-resistant pain, diagnostic or therapeutic blocks, neuromodulation techniques, or other interventions may be considered in specialized centers. Their indication, however, depends on the etiology and must fit within an overall strategy.\n<\/p>\n\n<div class=\"bp-model\">\n  <h2 id=\"lecture-proposee-par-le-modele-blue-portance\">Reading proposed by the Blue Portance model<\/h2>\n  <p>\n    For pain in which a mechanical component is plausible, the analysis distinguishes five dimensions:\n  <\/p>\n  <ol>\n    <li><strong>Current stress:<\/strong> is there still compression, traction, vibration, or a loss of gliding?<\/li>\n    <li><strong>Consequences of past damage:<\/strong> does the nerve show a loss of function, hypersensitivity, or incomplete recovery?<\/li>\n    <li><strong>Timing:<\/strong> do the symptoms appear immediately or after a delay, and do they persist after the stress has been removed?<\/li>\n    <li><strong>Associated mechanisms:<\/strong> scar, muscle, joint, visceral, or nociplastic pain.<\/li>\n    <li><strong>Recovery capacity:<\/strong> alternation of support points, mobility, blood supply, biological background, and sleep quality.<\/li>\n  <\/ol>\n  <p>\n    This reading cannot be used to diagnose a neuropathy. It does, however, help distinguish what still stems from a modifiable mechanical stress, what may reflect the consequences of a nerve lesion, and what requires medical reassessment.\n  <\/p>\n<\/div>\n\n<p>\n  This framework invites us in particular to examine an everyday mechanical factor that is often overlooked: the sitting position.\n<\/p>\n\n<h2 id=\"9-ce-que-lassise-peut-et-ne-peut-pas-modifier\">9. What sitting can \u2014 and cannot \u2014 change<\/h2>\n\n<p>\n  The sitting position can increase local pressure, reduce the space at an interface, combine compression and tension, limit gliding, and prolong a stress without sufficient recovery. In a person whose nerve is vulnerable or recovering, these factors can therefore reproduce or worsen the symptoms.\n<\/p>\n\n<p>\n  Changing the seat can then reduce a mechanical component: shifting the support areas, reducing a focal concentration of pressure, encouraging micro-adjustments, and allowing stress to alternate. This can be particularly relevant when the pain clearly varies with position and decreases when the support changes.\n<\/p>\n\n<p>\n  On the other hand, a seat does not on its own repair demyelination, axonal loss, a neuroma, or a central lesion. Nor can it establish that pain is neuropathic. Its possible role is to modify the mechanical environment that loads a vulnerable area, not to replace medical evaluation and treatment.\n<\/p>\n\n<div class=\"bp-recognize\">\n  <h3>Clues suggesting a mechanical component that is still active when sitting<\/h3>\n  <ul>\n    <li>reproducible onset after a period of sitting;<\/li>\n    <li>worsening at a specific support area;<\/li>\n    <li>reduction when changing position or offloading;<\/li>\n    <li>variation with the shape, firmness, or stability of the seat;<\/li>\n    <li>recurrence after a relatively consistent length of time;<\/li>\n    <li>improvement when support becomes more variable.<\/li>\n  <\/ul>\n<\/div>\n\n<p>\n  Recognizing a mechanical component when sitting does not, however, resolve every situation. What remains is to locate precisely the boundary between neuropathic pain and nociplastic pain.\n<\/p>\n\n<h2 id=\"10-douleur-neuropathique-et-douleur-nociplastique-ou-se-situe-la-frontiere\">10. Neuropathic pain and nociplastic pain: where is the boundary?<\/h2>\n\n<p>\n  Neuropathic pain implies a lesion or disease of the somatosensory system. Conversely, nociplastic pain corresponds to altered nociception without clear evidence of tissue damage activating nociceptors or of a somatosensory lesion or disease sufficient to explain the pain <span class=\"bp-inline-ref\">(IASP; Kosek et&nbsp;al., 2016)<\/span>.\n<\/p>\n\n<p>\n  In practice, the two mechanisms can coexist. A peripheral neuropathy can produce lasting abnormal activity and promote central changes that spread or amplify the pain. This does not, however, automatically turn all chronic neuropathic pain into nociplastic pain. It is therefore necessary to determine whether the somatosensory lesion still explains the distribution and most of the clinical picture, or whether more diffuse mechanisms have been added <span class=\"bp-inline-ref\">(Colloca et&nbsp;al., 2017; Latremoliere &amp; Woolf, 2009)<\/span>.\n<\/p>\n\n<table aria-label=\"Difference between neuropathic pain and nociplastic pain\">\n  <thead>\n    <tr>\n      <th>Dimension<\/th>\n      <th>Neuropathic pain<\/th>\n      <th>Nociplastic pain<\/th>\n    <\/tr>\n  <\/thead>\n  <tbody>\n    <tr>\n      <td><strong>Core condition<\/strong><\/td>\n      <td>Lesion or disease of the somatosensory system<\/td>\n      <td>Altered nociception without a somatosensory lesion sufficient to explain the pain<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Distribution<\/strong><\/td>\n      <td>Neuroanatomically plausible<\/td>\n      <td>Often more diffuse, multifocal, or disproportionate<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Possible signs<\/strong><\/td>\n      <td>Sensory deficit, allodynia, paresthesias, weakness depending on the lesion<\/td>\n      <td>Widespread hypersensitivity, variability, fatigue, sleep disturbances depending on the situation<\/td>\n    <\/tr>\n    <tr>\n      <td><strong>Overlap<\/strong><\/td>\n      <td colspan=\"2\">The same person can have several pain mechanisms at the same time.<\/td>\n    <\/tr>\n  <\/tbody>\n<\/table>\n\n<p>\n  The next article will focus specifically on nociplastic pain and nervous system hypersensitization, so as not to confuse the central consequences of a neuropathy with a self-sustaining nociplastic mechanism.\n<\/p>\n\n<p>\n  In practice, this boundary is sometimes difficult to draw with certainty. Several hasty claims therefore deserve to be qualified.\n<\/p>\n\n<h2 id=\"11-controverses-et-limites-des-connaissances-actuelles\">11. Controversies and limits of current knowledge<\/h2>\n\n<div class=\"bp-controversy\">\n  <h3>What should not be claimed too quickly<\/h3>\n  <ul>\n    <li><strong>\u201cThe pain burns, so it is neuropathic\u201d:<\/strong> the verbal quality is not enough.<\/li>\n    <li><strong>\u201cThe EMG\/NCS is normal, so the nerve is intact\u201d:<\/strong> some focal or small-fiber damage may not be detected.<\/li>\n    <li><strong>\u201cImaging shows compression, so it is causing the pain\u201d:<\/strong> an anatomical abnormality can be asymptomatic.<\/li>\n    <li><strong>\u201cThe decompression was successful, so the pain should disappear immediately\u201d:<\/strong> biological recovery can be slow or incomplete.<\/li>\n    <li><strong>\u201cThe pain persists, so the operation failed\u201d:<\/strong> several mechanisms must be distinguished.<\/li>\n    <li><strong>\u201cNeuropathic pain is irreversible\u201d:<\/strong> some neuropathies recover partially or substantially, depending on the cause and severity.<\/li>\n    <li><strong>\u201cAll persistent pain becomes nociplastic\u201d:<\/strong> chronicity alone is not enough to change how the mechanism is classified.<\/li>\n  <\/ul>\n<\/div>\n\n<p>\n  Another limitation lies in the categories themselves. They are useful for organizing reasoning and choosing strategies, but real-life situations are often mixed. A patient may simultaneously have nerve damage, interface pain, a sensitive scar, deconditioning, and central hypersensitivity.\n<\/p>\n\n<p>\n  Once these limitations are acknowledged, they should not discourage analysis. On the contrary, they invite us to structure our reasoning around concrete questions.\n<\/p>\n\n<h2 id=\"12-consequences-pratiques-pour-comprendre-une-situation\">12. Practical implications for understanding a situation<\/h2>\n\n<p>\n  When pain may be neuropathic, several questions structure the analysis:\n<\/p>\n\n<ul>\n  <li><strong>Plausible cause:<\/strong> is there a lesion, disease, or event that could damage the somatosensory system?<\/li>\n  <li><strong>Distribution:<\/strong> does the pattern correspond to a nerve, a nerve root, or a central pathway?<\/li>\n  <li><strong>Function:<\/strong> is there a sensory, motor, or reflex deficit?<\/li>\n  <li><strong>Timing:<\/strong> did the pain begin before, during, or after the presumed causal event?<\/li>\n  <li><strong>Current mechanics:<\/strong> does a position, pressure, or movement still reproduce the symptoms?<\/li>\n  <li><strong>Persistence:<\/strong> does the pain continue after the stress has been removed?<\/li>\n  <li><strong>Associated mechanisms:<\/strong> is there scar, muscle, joint, visceral, or nociplastic pain?<\/li>\n  <li><strong>Course:<\/strong> is there recovery, stability, spread, or worsening?<\/li>\n<\/ul>\n\n<p>\n  In addition, new or progressive weakness, significant loss of sensation, saddle anesthesia, bladder or bowel (sphincter) dysfunction, or rapid worsening require urgent medical evaluation. Likewise, persistent pain after nerve surgery warrants reassessment in order to distinguish expected recovery, complications, and associated mechanisms.\n<\/p>\n\n<p>\n  Up to this point, the pain is explained by damage to the somatosensory system. Yet some chronic pain persists even though no lesion is sufficient any longer to explain all of the symptoms. Another mechanism then comes into play: nociplastic pain.\n<\/p>\n\n<div class=\"bp-takeaway\">\n  <h2 id=\"a-retenir\">Key takeaways<\/h2>\n  <ul>\n    <li>Neuropathic pain is caused by a lesion or disease of the somatosensory system.<\/li>\n    <li>Burning, an electric-shock sensation, or pain located near a nerve is not enough to establish the diagnosis.<\/li>\n    <li>The diagnosis combines a compatible history, a neuroanatomical distribution, sensory signs and, when possible, evidence of the damage.<\/li>\n    <li>After a lesion, the myelin, the axons, the Schwann cells, and the central circuits can remain altered over the long term.<\/li>\n    <li>Removing a compression does not guarantee that the pain will disappear immediately.<\/li>\n    <li>After pudendal decompression, recovery can be slow, partial, or complicated by other pain mechanisms.<\/li>\n    <li>Neuropathic pain can coexist with nociceptive and nociplastic components.<\/li>\n    <li>Changing the seat can reduce a stress that is still active, but does not on its own treat an established nerve lesion.<\/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>Is pain along the course of a nerve necessarily neuropathic?<\/summary>\n    <div class=\"faq-content\">\n      No. The nerve&#8217;s sheaths, its blood vessels, and the neighboring tissues can produce nociceptive pain. Classifying pain as neuropathic therefore requires a lesion or disease of the somatosensory system supported by the history, the distribution, and the examination.\n    <\/div>\n  <\/details>\n\n  <details>\n    <summary>Why do I still hurt after nerve decompression?<\/summary>\n    <div class=\"faq-content\">\n      The compression may have been removed while the myelin, the axons, or the sensory circuits have not yet recovered. Spontaneous activity of the injured fibers, a scar, a loss of gliding, or another source of pain can also contribute. A reassessment is necessary if the pain persists or gets worse.\n    <\/div>\n  <\/details>\n\n  <details>\n    <summary>Can pudendal nerve surgery succeed without immediately eliminating the pain?<\/summary>\n    <div class=\"faq-content\">\n      Yes. The procedure can free an area of entrapment, but nerve recovery can take time and remain incomplete. Pelvic pain is often multifactorial; other mechanisms may persist despite an anatomically satisfactory decompression.\n    <\/div>\n  <\/details>\n\n  <details>\n    <summary>Does a normal EMG\/NCS rule out neuropathic pain?<\/summary>\n    <div class=\"faq-content\">\n      No. EMG\/NCS mainly assesses the large fibers, and some damage may be too focal or may involve the small fibers. Its interpretation therefore depends on the nerve studied, the technique, and the clinical context.\n    <\/div>\n  <\/details>\n\n  <details>\n    <summary>Is neuropathic pain always chronic?<\/summary>\n    <div class=\"faq-content\">\n      No. It can appear acutely after a lesion or a procedure. It becomes chronic, however, when it persists beyond the expected recovery time and the nerve mechanisms remain active.\n    <\/div>\n  <\/details>\n\n  <details>\n    <summary>Can neuropathic pain go away?<\/summary>\n    <div class=\"faq-content\">\n      Yes, particularly when the cause is removed early and the nerve recovers. In other cases, however, recovery remains partial. In short, the course depends on the cause, the duration, the axonal damage, the biological background, and the associated 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 pain going?<\/h2>\n  <p>\n    The analysis is based on location, stresses, timing, 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. It cannot diagnose a nerve lesion remotely, evaluate the outcome of a procedure, or choose a treatment. Persistent or worsening pain after surgery should be discussed with the medical team involved.\n<\/p>\n\n<section class=\"bp-references\">\n  <h2 id=\"references-scientifiques\">Scientific references<\/h2>\n  <h3>Definition and diagnosis<\/h3>\n  <ol>\n    <li>Finnerup NB, Haroutounian S, Kamerman P, et al. <em>Neuropathic pain: an updated grading system for research and clinical practice.<\/em> Pain. 2016;157(8):1599\u20131606. doi:10.1097\/j.pain.0000000000000492.<\/li>\n    <li>International Association for the Study of Pain. <em>Identifying neuropathic pain in the clinic: a guide for clinicians.<\/em> Neuropathic Pain Special Interest Group.<\/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. doi:10.1097\/j.pain.0000000000000507.<\/li>\n    <li>Colloca L, Ludman T, Bouhassira D, et al. <em>Neuropathic pain.<\/em> Nature Reviews Disease Primers. 2017;3:17002.<\/li>\n    <li>Truini A, et al. <em>Joint European Academy of Neurology\u2013European Pain Federation\u2013Neuropathic Pain Special Interest Group guidelines on neuropathic pain assessment.<\/em> European Journal of Neurology. 2023;30(8):2177\u20132196.<\/li>\n  <\/ol>\n  <h3>Biological mechanisms of nerve injury<\/h3>\n  <ol start=\"6\">\n    <li>Bove GM. <em>Epi-perineurial anatomy, innervation, and axonal nociceptive mechanisms.<\/em> Journal of Bodywork and Movement Therapies. 2008;12(3):185\u2013190. doi:10.1016\/j.jbmt.2008.03.004.<\/li>\n    <li>Campbell JN, Meyer RA. <em>Mechanisms of neuropathic pain.<\/em> Neuron. 2006;52(1):77\u201392. doi:10.1016\/j.neuron.2006.09.021.<\/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>Kocot-K\u0119pska M, et al. <em>Peripheral mechanisms of neuropathic pain \u2014 the role of neuronal and non-neuronal interactions and their implications for topical treatment.<\/em> Pharmaceuticals (Basel). 2021;14(2):77.<\/li>\n    <li>Mackinnon SE. <em>Pathophysiology of nerve compression.<\/em> Hand Clinics. 2002;18(2):231\u2013241.<\/li>\n    <li>Menorca RMG, Fussell TS, Elfar JC. <em>Nerve physiology: mechanisms of injury and recovery.<\/em> Hand Clinics. 2013;29(3):317\u2013330.<\/li>\n    <li>Schmid AB, Fundaun J, Tampin B. <em>Entrapment neuropathies: a contemporary approach to pathophysiology, clinical assessment, and management.<\/em> Pain Reports. 2020;5(4):e829.<\/li>\n  <\/ol>\n  <h3>Treatment and the pudendal nerve case<\/h3>\n  <ol start=\"13\">\n    <li>Finnerup NB, Attal N, Haroutounian S, et al. <em>Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis.<\/em> Lancet Neurology. 2015;14(2):162\u2013173. doi:10.1016\/S1474-4422(14)70251-0.<\/li>\n    <li>Soliman N, et al. <em>Pharmacotherapy and non-invasive neuromodulation for neuropathic pain: a systematic review and meta-analysis.<\/em> Lancet Neurology. 2025;24(5):413\u2013428.<\/li>\n    <li>Mylle T, et al. <em>Surgical approaches for pudendal nerve entrapment: insights from a systematic review and meta-analysis.<\/em> Surgical Endoscopy. 2024;38(8):4160\u20134170. PMID: 38942945.<\/li>\n    <li>Andiman SE, et al. <em>Impact of treatment of pudendal neuralgia on pain: a systematic review and meta-analysis.<\/em> International Urogynecology Journal. 2025;36(1):35\u201358. PMID: 39607531.<\/li>\n<\/ol>\n  <h3>Further reading<\/h3>\n  <ul>\n    <li>Labat JJ, Riant T, Robert R, Amarenco G, Lefaucheur JP, Rigaud J. <em>Diagnostic criteria for pudendal neuralgia by pudendal nerve entrapment (Nantes criteria).<\/em> Neurourology and Urodynamics. 2008;27(4):306\u2013310.<\/li>\n  <\/ul>\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 Neuropathic Pain 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 When Does Nerve Damage Become Neuropathic Pain? Epistemic note \u2014 This article distinguishes [&#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":"Nerve Damage and Neuropathic Pain | Blue Portance","_yoast_wpseo_metadesc":"Neuropathic pain comes from a lesion or disease of the somatosensory nervous system. Diagnosis, evolution, persistence.","footnotes":""},"pathologie_secondaire":[],"effet_positif":[],"class_list":["post-8041","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>Nerve Damage and Neuropathic Pain | Blue Portance<\/title>\n<meta name=\"description\" content=\"Neuropathic pain comes from a lesion or disease of the somatosensory nervous system. 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