This article is part of the Expert Guide “Understanding Pain”.

Why Does Pain Persist When Everything Looks Normal? Nervous System Hypersensitization

Figure 1 — How protective pain gradually becomes chronic painChronic painPain is called chronic when it persists or recurs for more than three months. It may accompany an identified disease or be a condition in its own right.Read the full entry : Chronic pain. The transition to chronic pain is not a sudden event but a gradual process of nervous system adaptation. A protective response that is initially useful can become excessive, then persistent, when painful stimulation continues over time.

1. Pain without visible damage is not imaginary pain

The previous articles in this guide showed that pain can arise from established nerve damage or from a nociplastic mechanism involving altered nociceptionNociceptionNociception is the process by which the nervous system detects and encodes stimuli that are potentially damaging to tissues. It is not the same as pain, which is an experience.Read the full entry : Nociception without damage sufficient to explain it (Kosek et al., 2016). A third level of interpretation concerns, more specifically, the way the nervous system itself processes and amplifies pain-related information.

A person can therefore experience intense pain even though imaging shows no structural abnormality. This does not mean the pain is “all in the head.” Imaging detects structural lesions, not the functional state of the pain-processing system. Moreover, many abnormalities visible on MRI are found in people who are not in pain, while some very real pain is not accompanied by any identifiable abnormality.

A point of terminology should also be clarified: hypersensitization is not a fourth pain mechanism to be added to nociceptive, neuropathic, and nociplastic painNociplastic painNociplastic pain is pain arising from altered nociception, without clear evidence of tissue damage activating nociceptors, or of a lesion or disease of the somatosensory system sufficient to explain the pain.Read the full entry : Nociplastic pain. On the contrary, it can accompany each of these three mechanisms, as an acquired property of the nervous system.

Figure 2 — Hypersensitization is not a fourth mechanism. It is a possible development of nociceptive, neuropathic, or nociplastic pain. It is an acquired property of the nervous system, not a new category of pain — two people with the same cause may evolve differently depending on their degree of hypersensitization.

What remains is to understand precisely what this amplification mechanism involves.

2. What is central sensitization?

In concrete terms, this mechanism shows up in three main ways. First, allodyniaAllodyniaAllodynia is pain caused by a stimulus that is normally not painful: a light touch, the contact of clothing, gentle pressure. It is a descriptive clinical term: it describes what the person feels, without by itself designating a mechanism.Read the full entry : Allodynia: a normally non-painful contact, such as clothing rubbing against the skin, becomes painful. Second, hyperalgesiaHyperalgesiaHyperalgesia is an increased pain response to a normally painful stimulus. In other words, a stimulus that is already painful causes abnormally amplified pain. It is a descriptive clinical term that does not, on its own, designate a mechanism.Read the full entry : Hyperalgesia: a mildly painful stimulus triggers a disproportionate response. Finally, spreading: the pain extends beyond the area initially affected (Woolf, 2011; Latremoliere & Woolf, 2009).

These changes result from enhanced synaptic efficacy and reduced inhibitory mechanisms in the spinal cord and in the brain structures involved in pain processing. They can also be demonstrated experimentally with sensory testing and imaging techniques (Woolf, 2011).

Figure 3 — Why does the nervous system react faster and faster? Over time, the pain-triggering threshold can drop. Stimuli that were previously well tolerated gradually become painful, and responses are amplified.

This definition remains abstract, however, until we understand how a normal nervous system comes to settle into this state.

3. How does this mechanism become established?

A system that learns to respond more strongly

The central nervous system displays synaptic plasticity that is comparable, at the molecular level, to the plasticity underlying certain memory processes. Signaling pathways shared by central sensitization and long-term potentiation have been identified, which partly explains why repeated pain can leave a lasting trace in the nervous system (Ji et al., 2003; Latremoliere & Woolf, 2009).

The role of the limbic system

Corticolimbic circuits, particularly those linking the medial prefrontal cortex, the amygdala, and the nucleus accumbens, also contribute to the persistence of pain. Longitudinal studies have shown that the anatomical characteristics of these circuits, measured early after an episode of low back painLow back painLow back pain is pain in the lower back, located between the thoracolumbar junction and the gluteal fold. In the vast majority of cases it is described as common (non-specific): it is mechanical in origin and does not stem from a serious disease.Read the full entry : Low back pain, are associated with the later risk of transition to chronic pain (Vachon-Presseau et al., 2016). A genuine emotional component is therefore added to the sensory component, without the pain ceasing to be biological.

Possible, but not systematic, cortical reorganization

In addition, in amputees with phantom limb pain, reorganization of the cortical representation of the missing limb has been associated with the intensity of the pain experienced (Flor et al., 1995). This work, carried out in the very specific context of deafferentation, illustrates the capacity of the somatosensory cortex to remodel itself; it does not, however, support the claim that identical reorganization applies to all chronic pain.

Once established, these central mechanisms do not operate in isolation. They are part of a continuous flow of information coming from peripheral tissues, particularly fascia.

4. The role of fascia in transmitting mechanical signals

Fascia, the connective tissue that envelops muscles, bones, and organs, is richly innervated. According to some authors, it constitutes a genuine sensory organ capable of continuously transmitting information about tissue tension, pressure, and deformation (Schleip et al., 2012). One hypothesis proposed in the literature is that this connective network may function as a body-wide signaling system, although this hypothesis remains, at this stage, less firmly established than the mechanisms of central sensitization themselves (Langevin, 2006).

When the stresses applied to fascia remain continuous, localized, and poorly varied, for example during prolonged static posture, gliding between tissue layers may decrease. The sensory receptors in the area concerned are then stimulated repetitively rather than in varied ways. It is not necessarily the signal itself that is the problem, but its repetition and the little information it carries for the nervous system.

Taken in isolation, this observation describes a peripheral phenomenon. Combined with an already sensitized nervous system, however, it can feed a self-sustaining loop — one that, moreover, is not limited to the mechanical dimension alone.

Figure 4 — Why does this hypersensitivity persist? Hypersensitization rarely results from a single cause, but from the interaction between mechanical stresses, painful experiences, emotions, behaviors, insufficient recovery, and lack of variability.

Understanding this loop raises a practical question: can fear of movement, fueled by the pain itself, become one of its drivers?

5. Fear of movement can sustain the loop

The fear-avoidance model describes how a catastrophic interpretation of pain can lead a person to avoid it rather than gradually confront it. This avoidance, in turn, promotes deconditioning, stiffness, and reduced exposure to varied movement (Vlaeyen & Linton, 2000).

Education about pain mechanisms can change this trajectory. A controlled trial showed that a single educational session, with no accompanying physical exercise, could already change certain beliefs and certain aspects of physical performance in people with chronic low back pain (Moseley, 2004). This suggests that the cognitive component of pain cannot be separated from its mechanical component, and that acting on one can influence the other.

If fear of movement can feed the loop, the opposite question naturally arises: how can movement variability help ease it?

6. Why reintroduce mechanical variability?

Viewed more broadly, hypersensitization can be understood as a lasting imbalance between the nervous system’s protective mechanisms and its recovery mechanisms. As long as the two remain in balance, a protective response stays useful and temporary. When signals perceived as threatening keep recurring and recovery becomes insufficient, however, the system can remain on alert longer than necessary — to the point of settling into chronic overprotection, even in the absence of any current threat.

Figure 5 — When the system protects more than it recovers. Chronic pain appears when protective mechanisms remain activated over the long term while recovery mechanisms become insufficient to restore the balance.

Restoring this balance therefore does not rely on a single lever: mechanical variability, better-quality recovery, reduced hypervigilance, and a gradual return to activities all contribute together. Blue Portance focuses specifically on the first of these levers, mechanical variability, without claiming to cover the others in place of qualified professionals.

Reducing hypersensitization through this mechanical lever is not simply a matter of increasing the volume of activity. Above all, it involves diversifying the mechanical information transmitted to the nervous system, through gentle, frequent, and progressive movements rather than through a one-off, intense effort.

Postural micro-adjustments, shifts in weight-bearing, or small tilting movements can thus help restore a better distribution of stresses and promote fascial glidingFascial glidingFascial gliding is the relative movement of fascial layers against one another, and against neighboring muscles, nerves and vessels, with every movement of the body.Read the full entry : Fascial gliding. As a result, the signals transmitted to the nervous system become less repetitive and, potentially, less likely to be interpreted as a persistent threat.

This approach also fits alongside rehabilitation techniques based on graded exposure to movement and with therapeutic education about pain mechanisms, without replacing either one.

In the Blue Portance reading, an improvement when positions and weight-bearing become more varied is a biomechanical observation worth noting; it is not, however, a recognized sign of central sensitization.

A system capable of recalibrating

This imbalance is not fixed, however. The same plasticity mechanism that allows the nervous system to become more reactive also allows it, gradually, to return to more balanced functioning when reassuring, varied, and repeated experiences come to replace the signals perceived as threatening.

Figure 6 — The nervous system can regain its balance. Hypersensitization is not irreversible. Thanks to the plasticity of the nervous system, reassuring experiences, recovery, and variability allow the protective mechanisms to recalibrate progressively.

This recalibration nevertheless remains gradual and specific to each person: it depends on the regularity of the changes introduced, not on an isolated one-off effort. Nor does it remove the need for a medical evaluation when the situation warrants it.

This understanding does, however, have limitations that should be spelled out.

7. Limitations and controversies

The mechanisms presented here are documented separately in the scientific literature, but how they fit together precisely in a given person remains difficult to establish clinically. No routine test can currently measure a patient’s degree of central sensitization directly, and attributing pain to this mechanism remains, for the most part, a process of exclusion and of converging evidence rather than direct proof.

Furthermore, the hypothesis that the fascial network plays a role as a body-wide signaling system remains debated and less firmly established than the mechanisms of central sensitization themselves. It is a useful avenue for understanding, not a scientific certainty.

Once these limitations have been stated, they do not prevent concrete practical implications from being drawn.

8. Practical implications for understanding a situation

• Trigger: is the pain still associated with identifiable situations (position, movement, exertion), even if the response seems excessive?
• Distribution: has the pain spread beyond the area where it first appeared?
• Sensitivity: have light or usually non-painful contacts become sensitive?
• Variability: does the pain vary depending on the diversity of positions and weight-bearing?
• Behavior: has movement avoidance set in, and since when?
• Course: is the pain still linked to a trigger, or does it now appear spontaneously and at rest?

Pain that becomes spontaneous, migrates without an identifiable trigger, or persists at rest warrants reassessment, as it may signal a shift toward more self-sustaining pain — a situation addressed specifically in another article in this guide.

Note: this content explains general mechanisms. It cannot be used to diagnose a state of central sensitization remotely or to choose a treatment. Pain that persists, worsens, or changes in character should be discussed with a healthcare professional.

© 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.