This article is part of the “Understanding Pain” Expert Guide.
Foundational article — Blue Portance Knowledge BaseWhy Do I Hurt? Understanding the Mechanism of Pain
Pain is not direct proof of damaged tissue. It arises when a stress exceeds the adaptive capacity of a tissue: ligament, enthesis, muscle, fascia, or nerve. Specialized receptors (nociceptors) are then activated, and this signal, transmitted to the spinal cord and then to the brain, is integrated and interpreted there. This pathway explains three essential things. First, pain can appear without any lesion visible on diagnostic testing. Second, it can depend as much on the duration of the stress as on its intensity. Finally, it can be felt in a location different from the structure that actually triggered the signal.
A universal experience
When I get stung or put my hand on a hot plate, I instinctively understand why I feel pain. The same is true when I take a blow or fall on my backside. I then feel a burning sensation, a dull ache, or a pulling sensation whose cause is immediately understandable. In these situations, there is an identifiable event that seems to explain the pain.
But what happens when pain appears without any impact, without any burn, without any visible injury, and sometimes even without any abnormality found on diagnostic testing? Why can simply sitting gradually become painful? Why do some people feel burning, an electric shock, or a sensation of compression even though no obvious lesion is found? And above all: how can pain be felt in a location different from where the problem actually lies?
To answer these questions, we first need to understand what pain really is — and, before that, what it is for.
What is pain for?
Before it is a problem, pain is a protective mechanism. It alerts the body when a tissue is at risk of being damaged, or when it detects a potentially dangerous situation. Without pain, we would keep loading weakened tissues without realizing it: it is therefore an alarm system essential to survival.
Like any alarm system, however, it can become oversensitive, persist after the initial danger has gone, or react out of proportion to the actual situation.
What exactly is pain?
“An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.” (Raja et al., 2020 — IASP)
This definition is important: it shows that pain is not simply a signal mechanically sent by a tissue to the brain. It is an experience constructed by the nervous system from many pieces of information: the signals coming from the tissues, their biological context, and their mechanical environment. The state of the nervous system, as well as the emotional and cognitive context, also contribute to it.
Constructed does not mean imaginary. It means that pain results from the nervous system’s interpretation of very real information. Pain is therefore never solely “in the tissue,” but it is not solely “in the head” either. Rather, it results from an interaction between these different levels, and it remains, in all cases, a real experience for the person who feels it.
The IASP notably distinguishes two major components of this experience:
- The sensory (discriminative) component — 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.
- The emotional component — 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.
Three mechanisms that produce pain
Before going into detail, it is useful to know that pain can result from three main mechanisms, which are not mutually exclusive. The nociceptive mechanism corresponds to the activation of nociceptors by tissue stress. Damage to or a disturbance of the somatosensory nervous system itself defines the neuropathic mechanism. As for the nociplastic mechanism, it corresponds to altered processing of pain information, without any demonstrated lesion or nerve damage.
The article “Nociceptive, Neuropathic, and Nociplastic Pain” describes each of these mechanisms in detail, along with their boundaries, their possible overlaps, and concrete illustrations.
Pain and suffering: two different realities
Pain is a biological signal. Suffering corresponds to what this signal produces in the person’s life: worry, limitation of activities, fatigue, loss of confidence, isolation. Both are real. But they do not arise from exactly the same mechanisms — and this is, in fact, the distinction partly covered by the emotional component mentioned in the IASP definition. Understanding this difference avoids reducing a person’s entire life to their pain signal alone, while taking seriously what they are going through.
Which tissues actually trigger pain?
When we talk about pain in the tailbone, the perineumPerineumThe perineum is the region at the lower part of the pelvis, between the thighs. It includes skin, muscle, fascial, vascular and nerve structures, and it is also an area that may bear load when sitting.Read the full entry : Perineum, or the sitting bones, we often imagine that it is the bone that hurts. In reality, bone is rarely the painful structure. It is mainly the surrounding living tissues, rich in sensory receptors, that can trigger a pain signal when they are loaded beyond their adaptive capacity. Depending on the situation, these may include:
- a joint capsule;
- a ligament;
- an enthesis (the area where a tendon or muscle attaches to bone);
- a fasciaFasciaFascia are connective tissue structures that envelop, connect or separate certain parts of the body. The "fascial system" refers to a broader set of connective tissues considered in their functional continuity.Read the full entry : Fascia;
- a muscle or a tendon;
- an intervertebral discIntervertebral discThe intervertebral disc is a fibrocartilaginous structure located between two vertebral bodies. Made up of a gel-like nucleus surrounded by a fibrous ring, it transmits and distributes loads while allowing the spine to move.Read the full entry : Intervertebral disc;
- a nerve structure;
- more rarely, the bone itself, when there is genuine bone involvement (a fracture, for example).
These tissues do not all have the same adaptive capacity. This is why the same stress can be perfectly well tolerated by some tissues while it becomes painful for others: each tissue has its own mechanical properties and its own sensitivity. This point is essential, because a single pelvic movement can load several tissues at once. One of them can then become the main pain generator, without the others necessarily being involved.
Depending on the situation, pain can result from compression, stretching, shearShearShear is a deformation produced by forces parallel or tangential to a surface, which cause neighboring layers or regions of a tissue to slide relative to one another.Read the full entry : Shear, or friction. It can also stem from a loss of gliding between two tissues or from excessive traction on an attachment. So it is not only the tissue involved that matters, but also the nature of the stress it is subjected to.
From stress to pain: a chain, not a shortcut
Contrary to a very widespread belief, mechanical stress never directly produces pain. It first acts on a tissue. That tissue has its own adaptive capacity: its ability, at any given moment, to absorb this stress without damage and without an alarm signal. As long as the stress stays within the limits of this capacity, nothing happens consciously.
When the stress exceeds this adaptive capacity, the tissue’s nociceptors are activated: these are specialized sensory receptors capable of detecting a potential threat to its integrity. They then transmit information to the spinal cord and then to the brain, which integrates and interprets it in its context. It is this interpretation that can produce the experience we call pain.
What this chain explains
This chain explains why the same stress can be perfectly well tolerated by one person and painful for another. The difference does not lie in the stress itself, but in the adaptive capacity of the tissue that receives it, at that precise moment. Figure 3 then illustrates how this chain naturally unfolds depending on whether the tissues’ adaptive capacity is preserved or exceeded.
It is this mechanism — the activation of nociceptors by a stress that exceeds a tissue’s adaptive capacity — that is called nociceptive painNociceptive painNociceptive pain is pain related to actual or threatened damage to non-neural tissue, resulting from the activation of nociceptors. The somatosensory nervous system is functioning normally.Read the full entry : Nociceptive pain. It accounts for the majority of sitting-related pain.
The chain in a diagram
Why duration changes everything
Time is a variable just as important as the intensity of the stress itself. The same stress, if very brief, can be perfectly well tolerated by a tissue. Repeated or sustained for several tens of minutes, however, that same stress can gradually exceed its tissue adaptive capacity. This principle explains why a sitting position that is comfortable at first can become painful after a certain time. Yet no 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 has ended up exceeding what the tissue could absorb.
Frequency of repetition is a third essential variable, on a par with intensity and duration. A moderate stress, repeated hundreds of times a day, can produce the same consequences as a much more intense but one-off stress. In that case, the tissue no longer has the time it needs to recover between two loading episodes.
An essential dissociation: where it hurts is not always where it comes from
This chain has a direct consequence, and it is probably the most counterintuitive idea in this article. The brain generally localizes pain at the sensory nerve endings that transmitted the signal. This is not necessarily where the structure that actually triggered the signal is located. Irritation occurring at one point along a nerve’s course can therefore be felt farther away, across all or part of its distribution territory.
This is not a matter of adding a component to the IASP definition, which remains the reference. Rather, it is a complementary interpretive principle specific to this biomechanical model. It can be called a principle of anatomoclinical dissociation between the site where the stress originates and the site where the pain is perceived.
The origin of the signal can also lie directly along the course of the nerve itself — compression, an adhesion limiting its gliding, prolonged irritation. When this is the case, rather than in a peripheral tissue that the nerve supplies, this is referred to as neuropathic painNeuropathic painNeuropathic pain is pain caused by a lesion or disease of the somatosensory nervous system.Read the full entry : Neuropathic pain. It stems from damage to or a disturbance of the somatosensory nervous system, and not from the simple activation of nociceptors by tissue stress.
Illustration: the pudendal nerve and Alcock’s canal
The example of pudendal neuralgiaPudendal neuralgiaNeuropathic pain in the territory of the pudendal nerve (perineum, external genitalia, anal region), often made worse by sitting.Read the full entry : Pudendal neuralgia is particularly instructive. As it exits Alcock’s canal, the pudendal nervePudendal nerveThe pudendal nerve arises mainly from the sacral roots S2 to S4. It provides a large share of the sensory and motor innervation of the perineum and the external genitalia.Read the full entry : Pudendal nerve divides into three branches. The first runs toward the clitoris or penis. The second in turn subdivides toward the urethra on the one hand, and the labia or scrotum on the other. Finally, the third runs toward the anal canal.
The pain is perceived at these nerve endings, across all three territories or partially in one of them. The origin of the problem, however, most often lies much farther upstream, precisely at Alcock’s canal. It may be compression of the nerve, fibrosis, or an adhesion that blocks its normal gliding. In summary:
Origin (Alcock’s canal) → Transmission → Perception (anus · vulva or penis · urethra)
The brain does not always localize pain at the structure responsible for it. It localizes it at the nerve endings that signaled it.
Can I be in pain without an apparent cause?
Yes. But that does not mean the pain is imaginary. Several situations, which are not mutually exclusive, can explain it:
Four common situations
- The mechanical cause is very subtle — an adhesion, micro-instability, or muscle hypertoniaHypertoniaHypertonia refers to an increase in muscle tone or in resistance to passive movement. The term does not describe a single cause: depending on the context, it may reflect a neurological disorder, increased muscle activity, difficulty relaxing, tissue stiffness or a protective strategy related to pain.Read the full entry : Hypertonia cannot be seen with the naked eye and may go unnoticed during a standard examination.
- The cause is distant from the site where pain is felt — as in the example of Alcock’s canal, where origin and perception do not coincide.
- The tissues have become hypersensitive — 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.
- The test results are normal — 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.
This article answers the question: why does pain appear?
Why does some pain become chronic?
In some situations, the tissue that was initially loaded partially recovers, while the nervous system remains more reactive. This is called sensitization, which can be peripheral (at the level of the tissues) or central (at the level of the nervous system itself).
In some cases, a nociplastic component can also emerge. This is pain related to altered processing of pain information. No tissue damage or involvement of the somatosensory system is then sufficient to explain it (Kosek et al., 2021). This mechanism mainly concerns certain 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 conditions that have persisted for several months; it generally does not explain the initial onset of mechanical sitting-related pain.
What this does not mean
- Pain without a visible lesion is not pain that is “all in your head.”
- A normal test result does not mean that no mechanism explains it.
- Pain felt far from its actual origin is not a perception error to be corrected, but information to be interpreted correctly.
- Chronic or sensitized pain is not exaggerated pain: it is an alarm system whose settings have changed.
Pain is a message. Understanding that message is often more important than trying to silence it.
— Blue Portance biomechanical model
Key takeaways
- Pain is an experience constructed by the nervous system — constructed does not mean imaginary.
- It arises when a stress exceeds the adaptive capacity of a tissue: ligament, enthesis, muscle, fascia, or nerve, and rarely the bone itself.
- The duration of a stress matters as much as its intensity.
- The site where pain is felt is not always the site where the problem lies.
- Pain without an apparent cause is not pain without a cause — and chronic pain is not exaggerated pain.
Further reading
Related frequently asked questions
Can I be in pain without an apparent cause?
Why can pain be felt in a location different from its origin?
Does a normal imaging test rule out a real cause for the pain?
What is the difference between pain and suffering?
Do you recognize your situation?
Understanding the mechanism behind your pain is the first step toward analyzing it correctly.
Analyze my situation →Note: this content aims to explain general pain mechanisms. It does not constitute a medical diagnosis or a prescription, and it does not replace the advice of a healthcare professional.
Scientific references
- Raja SN, Carr DB, Cohen M, et al. The revised International Association for the Study of Pain definition of pain: concepts, challenges and compromises. Pain. 2020;161(9):1976–1982.
- International Association for the Study of Pain (IASP). IASP Terminology — Pain Definition. 2020.
- Kosek E, Cohen M, Baron R, et al. Chronic nociplastic pain affecting the musculoskeletal system: clinical criteria and grading system. Pain. 2021;162(11):2629–2634.
Further reading
- Basbaum AI, Bautista DM, Scherrer G, Julius D. Cellular and Molecular Mechanisms of Pain. Cell. 2009;139(2):267–284.
- Treede RD. The role of quantitative sensory testing in the prediction of chronic pain. Pain. 2019;160 Suppl 1:S66–S69. doi:10.1097/j.pain.0000000000001544.
© 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.
