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

Why Does Pain Continue When Nothing Seems to Explain It Anymore? Neurosensory Deprogramming

What this article proposes

Figure 1 — From triggered pain to autonomous pain. The transition to chronic pain is generally a gradual process. The pain response becomes less and less dependent on the initial trigger, and increasingly sustained by the nervous system’s adaptation mechanisms.

1. A question that follows on from the previous article

The previous article showed how a nervous system can become hypersensitive. It then lowers its triggering threshold, amplifies signals, and spreads them beyond the initial area (Woolf, 2011). In that interpretation, the pain nevertheless remains tied to an identifiable trigger, even if the response is disproportionate.

One question nevertheless remains open. In some people, the pain continues to exist even though no mechanical trigger, no residual lesion, and no inflammatory context is sufficient to explain it any longer. It may thus appear at rest, at night, or move from one area of the body to another. This situation therefore does not fall under neuropathic pain, which requires a demonstrated lesion of the somatosensory system. Nor is this apparent loss of a trigger, on its own, sufficient to establish nociplastic pain in the IASP sense, even though it comes close to it (Kosek et al., 2016). It therefore raises a more specific question: why does a system that has become hypersensitive stop, in some people, depending on a trigger in order to keep producing pain?

It is precisely this question that the neurosensory deprogramming model seeks to shed light on.

2. What is meant by neurosensory deprogramming?

The term, as passed on by Pierre Ivaldi

In Pierre Ivaldi’s clinical practice, neurosensory deprogramming refers to a change observed in some patients suffering from chronic pain. The pain then gradually ceases to be tied to an identifiable mechanical, postural, or lesion-related trigger, and seems to take on a form of autonomy of its own. The term itself is not a diagnostic category recognized by the IASP in the way that nociceptive, neuropathic, or nociplastic pain are. It is instead a clinical observation, named by its originator over the course of his day-to-day work with patients in functional rehabilitation.

The explanatory hypothesis proposed by Blue Portance

In concrete terms, this loss of calibration corresponds to a point in the course of events at which the nervous system no longer merely amplifies a signal it receives. It comes to sustain pain activity that is relatively independent of the sensory information actually reaching it. This does not settle the question, still debated in the literature, of whether a nervous system can produce pain that is entirely independent of any sensory input (Clark, 2013).

Figure 2 — Neurosensory deprogramming. In the Blue Portance model, it corresponds to a progressive loss of capacity. The nervous system is less and less able to make proper use of the sensory information it actually receives in order to adjust its response to reality.

Understanding this hypothesis of a loss of calibration first requires revisiting the documented biological mechanisms that make it plausible.

3. Which documented mechanisms does this model draw on?

Hyperexcitability that can become self-sustaining

Central sensitization, already described in the previous article, can progress to lasting hyperexcitability of neurons in the dorsal horn of the spinal cord. Some neurons may then display spontaneous activity, independent of any current peripheral stimulation. This occurs in particular when the inhibitory mechanisms that normally dampen pain transmission become less effective (Latremoliere & Woolf, 2009).

The engram concept applied to pain

Among the mechanisms discussed in this article, that of engrams is receiving particular attention in the recent literature. On its own, it does not constitute the explanation of the model: it supports the broader hypothesis of a loss of calibration, alongside the other mechanisms presented below. An engram refers to the physical trace, in neural circuits, that a learning process or an experience leaves in the nervous system.

In addition, recent work in animal neuroscience has shown that prefrontal circuits can store a lasting trace associating fear and pain. In mice, specifically disrupting this engram reduces established pain hypersensitivity without acting on the initial lesion (Stegemann et al., 2023). This work remains preclinical and does not support the claim that an identical mechanism explains chronic pain in humans. It nevertheless provides a plausible framework for understanding how a painful experience could, in some people, become durably consolidated in brain circuits rather than fading away.

The anterior cingulate cortex: shared plasticity

The anterior cingulate cortex, in particular, displays forms of synaptic plasticity. These are involved both in the affective component of pain and in certain memory processes (Bliss et al., 2016). This overlap between pain circuits and memory circuits is thus today one of the most active lines of research for understanding the persistence of chronic pain.

Figure 3 — Pain engrams. A painful experience can leave a lasting trace in neural networks, one that can be reactivated even in the absence of the initial trigger.

Reorganization of resting-state brain networks

In people with chronic 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, alterations in the functional connectivity of the default mode network have been reported (Baliki et al., 2008). This network comprises the circuits that are active when the brain is not engaged in a specific task. Longitudinal studies have also shown that certain characteristics of connectivity between the prefrontal cortex and the striatum, measured early on, are associated with the later risk of transition to chronic pain (Baliki et al., 2012). These findings extend the observations on the role of the limbic system already presented in connection with hypersensitization (Vachon-Presseau et al., 2016).

Predictive coding: a theoretical hypothesis, not an established fact

Some researchers propose that the brain does not merely process sensory signals passively. It continuously generates predictions that it compares with incoming inputs, including for pain (Clark, 2013; Büchel et al., 2014). This predictive coding hypothesis thus offers an interesting theoretical framework. An expectation of pain, once sufficiently entrenched, could weigh on perception in the same way as a real signal. It is, however, one theoretical framework among others in cognitive neuroscience, and not a physiological mechanism unequivocally demonstrated for chronic pain in humans.

What these mechanisms suggest, taken together

Taken together, these mechanisms do not demonstrate that a nervous system can produce pain completely cut off from all bodily information. They do, however, converge on a single idea. Beyond a simple lowering of the triggering threshold, something else seems to become progressively dysregulated. That something is the nervous system’s ability to make proper use of the sensory information it actually receives in order to adjust its response. It is this hypothesis that the neurosensory deprogramming model sets out to explore.

Figure 4 — The scientific foundations of the Blue Portance model. The model does not rest on a single mechanism, but on the integration of several processes that are now widely documented in neuroscience.

Figure 5 — How pain can persist in the absence of a trigger. The Blue Portance model shows that no single mechanism is sufficient on its own to explain this persistence. Their combination, however, can sustain pain long after its initial cause has disappeared.

With this interpretation laid out, it still needs to be clearly distinguished from the mechanisms already defined in this guide — otherwise, confusion would be easy.

4. How does this model differ from the mechanisms already defined in this guide?

On the one hand, neuropathic pain requires a demonstrated lesion or disease of the somatosensory system. On the other hand, nociplastic pain corresponds to altered 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 sufficient evidence of tissue or nerve damage. It is nevertheless defined by the IASP as a mechanism in its own right, regardless of how long it has been present (Kosek et al., 2016).

Neurosensory deprogramming, as proposed by Blue Portance, therefore does not replace either of these two categories and does not constitute a fourth diagnostic category. Rather, it describes an additional level of interpretation. This level applies in particular when pain — originally neuropathic, nociplastic, or mixed — seems to have gradually lost its link with an identifiable trigger. It is therefore not a competing mechanism, but a way of interpreting how already recognized mechanisms evolve over time.

With this distinction made, a practical question remains: how can one recognize, in a real clinical picture, that pain has drifted away from its initial trigger?

5. Which clues point toward this model?

None of these features, taken in isolation, is sufficient to reach a conclusion. As with nociplastic pain, this is a body of converging clinical evidence, not a biological test or an imaging study that allows direct confirmation.

6. Which approaches are mentioned in the literature?

The aim here is not to propose a treatment protocol: this article is not intended to take the place of one. It is rather to outline the main families of approaches discussed in the scientific literature for what Pierre Ivaldi called neurosensory reprogramming. This term refers to the nervous system’s ability to gradually rebuild a response that is more accurately calibrated to the sensory information it actually receives.

Graded exposure below the pain threshold

Stimulation that systematically triggers pain tends to confirm, for the nervous system, the association between movement and threat. Conversely, a gradual reintroduction of movements below that threshold can reduce fear of movement. This approach follows directly from the fear-avoidance modelFear-avoidance modelThe fear-avoidance model describes the possible relationships between how a person interprets pain, fear, avoidance and activity restriction. It is an explanatory model, not a diagnosis.Read the full entry : Fear-avoidance model already presented in this guide (Vlaeyen & Linton, 2000).

Mirror therapy and graded motor imagery

These approaches, originally developed for phantom limb pain, harness the plasticity of the body’s cortical representation (Ramachandran & Rogers-Ramachandran, 1996; Flor et al., 2006). A controlled trial thus showed a greater reduction in pain than that achieved with standard care. It involved people with phantom limb pain or complex regional pain syndrome (Moseley, 2006). This result was broadly corroborated by a later systematic review covering broader chronic pain populations (Bowering et al., 2013).

Neurofeedback

This approach aims to train a person to voluntarily modulate certain parameters of their brain activity, displayed in real time. A randomized trial in people with fibromyalgiaFibromyalgiaFibromyalgia is a chronic pain syndrome combining persistent widespread pain, fatigue, sleep disturbances and often difficulty concentrating, with no tissue damage that could on its own explain the intensity of the symptoms.Read the full entry : Fibromyalgia reported an improvement in pain and in several associated symptoms. This improvement was comparable to that achieved with a standard drug treatment (Kayiran et al., 2010). The available data nevertheless remain limited in the number of studies.

Mechanical variability, a complementary lever

As mentioned in the previous article, poor and repetitive mechanical information can help sustain a nervous system that is already hypersensitive (Langevin, 2006). Reintroducing postural variabilityPostural variabilityPostural variability refers to fluctuations in posture over time. It is measured in particular through displacements of the center of pressure and is neither good nor bad in itself.Read the full entry : Postural variability therefore does not directly target a consolidated pain engram, but it may reduce one of the sources of signals likely to sustain it.

All of these approaches share one thing in common: none of them acts alone on all the levels involved. Managing this type of clinical picture therefore calls for multidisciplinary care, not a single technique applied on its own.

As with the previous articles in this guide, this interpretive framework, presented above, calls for a caveat regarding its limitations.

7. Limitations and controversies

Another limitation lies in the very nature of the research field. A large part of what this model draws on — engrams, predictive coding — comes from recent, sometimes preclinical, work. On these specific points, the scientific consensus remains considerably less established than for central sensitization or the IASP definition of nociplastic pain.

8. Practical implications for understanding a situation

• Trigger: does the pain remain linked to an identifiable mechanical or postural factor, even if amplified?
• Timing: does it now appear at rest, at night, or in the absence of any load or activity?
• Distribution: does it migrate from one area to another without anatomical consistency?
• History: is there a significant emotional context associated with the onset or worsening of the pain?
• Resources: which levers — gradual movement, variability, specialized support — have not yet been brought into play?

Rapid worsening, the appearance of new neurological signs, or a decline in general health changes the picture. However long-standing the pain, these signs should prompt a medical reassessment without delay.

Neurosensory deprogramming is not presented here as an irreversible state. Plasticity mechanisms allow the nervous system to gradually drift away from adaptive functioning. But this same plasticity is also the biological basis of what Pierre Ivaldi called neurosensory reprogramming. This does not correspond to an “erasure” of previous circuits. It is rather a new, gradual learning process that allows the nervous system to rebuild a response more accurately calibrated to the sensory information it receives.

Figure 6 — Possible pathways to neurosensory reprogramming. Recovery does not generally rely on a single intervention, but on the combination of several levers acting at different levels of the nervous system.

Note: this content explains general mechanisms and an interpretive model specific to Blue Portance. It cannot be used to diagnose neurosensory deprogramming remotely or to choose a treatment. Chronic pain with no identifiable trigger should be discussed with a healthcare professional.

© 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.