The relationship between injury and pain – the mainstream view
In “How to treat pain #1”, I explained why understanding pain is fundamental to treatment. I claimed that mainstream pain scientists and theorists are mistaken about pain’s function and, therefore, treatment based on mainstream scientific theory is not as effective as it might be. I gave one reason for my claim, sensory inaccuracy. Quite simply, if pain did function as the conscious awareness of noxious stimuli (i.e. stimuli that are damaging or threatening to damage tissue), then we should expect a strong correlation between pain and (putative) stimulus. But the evidence is that the correlation between pain and noxious energy is weak. Sensory inaccuracy is inconsistent with evolutionary theory.
The claim that scientists are mistaken about pain’s function is a big claim, which requires proper justification. In the second part of the tutorial I explain mainstream functional theory in greater detail, and in the next part I will provide more reasons for, and briefly discuss the neuroscientific implications of, rejection.
2.1 Injury and pain – a direct causal relationship?
Causation is fundamental to pain treatment for the simple reason that:
You cannot affect a pain without affecting a cause of that pain.
So treatment is wholly ineffective unless it affects a cause or causes of pain.
Here, I refer to the facts about cause: you cannot affect a pain unless you affect an actual cause of that pain. The importance of understanding is now clear. Effective treatment requires you to understand the facts about pain. So the aim of pain education is to foster beliefs that correspond with facts (i.e. true beliefs). False beliefs (i.e. beliefs that do not correspond with facts) give rise to ineffective treatment. The question, What are the causes of pain? is, then, fundamental to effective pain treatment.
It is commonly believed that injury directly causes pain, that when you feel a pain you are feeling tissue damage. The facts that we tend to experience pain more frequently when we are injured and that this frequency tends to ease as tissue heals provide reasons to accept this view, but there are compelling common sense reasons for rejection.
Simple observation provides one good reason. It is easy to ignore the fact that pain is an everyday experience. For example, you feel pain if you sit for too long in one position, or someone pulls your hair, or you grab the handle of a hot pain. In these everyday examples, there is no tissue damage so tissue damage cannot be the cause of these pains.
The intermittent nature of most episodes of pain is another reason. If tissue damage caused pain, we would experience continuous pain (that eases in intensity as tissue heals) for the whole period when a tissue is damaged. But most episodes of continuous pain are abnormal. When injured it is normal for pain to be intermittent, for pain to disappear and reappear, to become more or less intense, with changes in activity, posture, etc..
These common sense reasons to accept that tissue damage is not a direct cause of pain are supplemented by a straightforward yet persuasive scientific reason. Quite simply sensory nerves (i.e. sensory ‘neurons’) detect only energy. As damaged tissue is a tissue state, the state of being damaged, and tissue damage is not a type of energy, the sensory neurons involved in pain cannot detect tissue damage.
2.2 Pain science – the indirect causal relationship between injury and pain
The mainstream science is that pain has multiple causes. These causes are often classified under the biological, psychological, and social categories that together comprise the ‘biopsychosocial’ label. Although the biopsychosocial take on multiple cause is central to the mainstream approach to pain treatment, multiple cause would be a confusing topic at this stage of the tutorial so it will be ignored. I want to begin by concentrating on a particular biological cause: the detection of a noxious stimulus by specifically adapted sensory neurons. These sensory neurons are called ‘nociceptive neurons’.
The International Association for the Study of Pain (a very important organisation) define a noxious stimulus as a “stimulus that is damaging or threatens damage to normal tissues” (IASP, 2017), but this is rather muddled. It is best to think of a noxious stimulus as energy at a bodily location that is having two simultaneous effects:
A The noxious effect – energy is damaging or threatening to damage tissue, and
B The stimulating effect – that energy is being detected by a nociceptive neuron (where a nociceptive neuron is a sensory neuron specifically adapted to detect energy at intensities that are damaging or threatening to damage tissues).
Energy is noxious if it satisfies A; i.e. energy is having a noxious effect. But energy is only a noxious stimulus if it satisfies A and B; i.e. energy is having both noxious and stimulating effects. From this, the orthodox scientific theory is that pains are normally caused by detection of noxious energy by a nociceptive neuron.
As energy at a bodily location is sometimes intense enough to threaten damage but not intense enough to cause damage, mainstream theory is consistent with the evidence that pain is often experienced when no injury is occurring or present (i.e. when you sit for too long in one position, or someone pulls your hair, or you grab the handle of a hot pain, etc.). And the reason it is not normal to experience pain continuously when you are injured is that the normal cause of pain is noxious energy not damaged tissue.
The concept of tissue threatening is complicated and, because it adds nothing of consequence to the coming explanation, will be ignored for the purpose of understanding.
2.3 What is noxious energy?
Despite the simplification, I cannot pretend that the concept of noxious energy (i.e. tissue damaging energy) is straightforward. The distinction between noxious energy and a noxious stimulus is part of the complexity. (This is the distinction between energy that satisfies A and energy that satisfies A & B in 2.2, above.) You also need to understand two other aspects of this complexity. First, noxiousness is not an intrinsic property of energy like type (e.g. thermal energy) and intensity (e.g. 40°C). Noxiousness is a relational property involving intrinsic properties ofenergy and something I call the ‘damage threshold’ which is a relational property of the tissues. The second complexity is that the damage threshold varies.
The damage threshold is:
Damage threshold The lowest intensity at which energy can damage tissue at a bodily location.
Like noxiousness, the damage threshold is determined by a relationship between energy and the tissues; specifically, between the biological properties of tissue at a particular bodily location (‘L’) and intrinsic properties of energy (type and intensity). The difference between the two is that ‘noxious’ refers to a relational property of energy, and ‘damage threshold’ refers to a relational property of bodily tissue.
Noxious energy is:
Noxious energy Energy at L that exceeds the damage threshold of tissue at L.
This gives two conditions on energy qualifying as noxious:
- Energy must be located at L.
- Energy must exceed the damage threshold at L.
Energy is noxious if and only if it satisfies both (i) and (ii) (see A and B in 2.2).
To illustrate the relational nature of noxiousness, there is a tendency to think of the flame of a gas stove as harmful. For practical purposes this is a helpful belief, but in the context of this tutorial it will mislead. A flame is not necessarily harmful because it is not intrinsically noxious. The flame has the potential to cause harm because of the intrinsic properties of its thermal energy and the intrinsic (biological) properties of living tissues. As the intensity of the thermal energy exceeds the damage threshold at L, the flame satisfies condition (ii) but not (i). Therefore, the flame is not intrinsically harmful. (To emphasise the relational point, the flame would not even have the potential to harm if living tissue were extremely resistant to thermal energy.) The energy is only actually harmful if another condition is met: the flame must be sufficiently close to living tissue to elevate tissue temperature above the damage threshold. In which case it would satisfy (i) and (ii).
While it is obvious that the intensity of energy at L could rise above or fall below the damage threshold at L, it is the variability of the damage threshold of the tissue at L that really complicates matters. The damage threshold varies with tissue use (most tissues get stronger or weaker with the degree of use) and tissue health, but I’m going to ignore these causes of variability. In the context of most treatment, the key point is that the damage threshold falls with tissue damage and rises with tissue healing.
2.4 Nociceptive neurons and the detection of noxious energy
The mainstream understanding that pain has the sensory function of making us consciously aware that a stimulus is noxious imposes a particular demand on the pain system: the pain system must have some means of determining, with a reasonable degree of accuracy, whether energy at L exceeds the damage threshold at L. According to mainstream science this task is performed by the specifically adapted nociceptive neurons mentioned above. For functional efficiency this requires the population of neurons at L to have the following properties:
1 At least some nociceptive neurons at L have stimulus thresholds at the damage threshold.
2 No nociceptive neurons in the vicinity of L have stimulus thresholds below the damage threshold.
The stimulus threshold is:
Stimulus threshold The lowest intensity of energy that a neuron can detect.
Mainstream science is committed to 1 and 2 for these reasons. The pain system would be functionally inefficient if, in contradiction of 1, all nociceptive neurons at L had stimulus thresholds in excess of the damage threshold but none had stimulus thresholds at the damage threshold. This would mean that a significant proportion of events involving low intensities of noxious energy (remember, by definition, low intensities of noxious energy damage tissue) would escape detection by the pain system. Therefore, there would be no pain to make us aware that energy is having a noxious effect. This sensory inaccuracy would represent a surprising evolutionary oversight, so it is reasonable to assume 1.
In contradiction of 2, if some nociceptive neurons had stimulus thresholds below the damage threshold, functional efficiency would require the pain system to have some means, other than the sensory neurons of the nociceptive system, of discriminating between noxious and non-noxious stimuli. Pain scientists have not identified such a mechanism, all their eggs are firmly in the nociceptive basket, so 2 is an important (if hidden) constituent of mainstream pain neuroscience.
It is easy to accommodate 1 and 2 into a theoretical scheme in which the damage threshold is fixed. Quite simply, evolutionary pressures determine that the lowest nociceptive stimulus threshold at L is the same as the damage threshold at L. However, this explanation will not suffice for variable damage thresholds because nociceptive thresholds would be fixed (by evolutionary pressures).
How does the pain system match stimulus thresholds with damage thresholds when damage thresholds vary with tissue damage and healing?
Biology provides an answer: tissue in the vicinity of damage releases biochemicals (collectively known as ‘algogenic’ or ‘pain-promoting’ substances) that lower the stimulus thresholds of neurons. As tissue heals less algogenic substance is released, so the stimulus thresholds of nociceptive neurons vary with damage and healing.
In summary of this important point, in the presence of tissue damage and healing, the damage thresholds of tissue at L and the stimulus thresholds of sensory neurons at L both vary. The increased sensitivity of nociceptive neurons to lower intensities of energy (caused by algogenic substance release) explains how actions and positions that were not painful in the uninjured state become painful when injury is present. And diminishing algogenic substance release explains how pain resolves with tissue healing.
2.5 Summary
Even in a simplified state the content of this second part of the tutorial is difficult. There are lots of definitions: ‘damage threshold’; ‘noxious threshold’; ‘stimulus threshold’; ‘noxious energy’; ‘noxious stimulus’; and so on. Much of this may seem irrelevant, but it is not. The fact that mainstream science provides definitions of a ‘noxious stimulus’ and a ‘nociceptive neuron’ boil down to the claim that noxious energy is detected by sensory neurons. This claim is a fundamental aspect of mainstream functional theory: as pain functions as the conscious awareness of noxious stimuli, the biological system that generates pain (the ‘pain system’) must have some means of detecting noxious energy. The job of detection is done by a specifically adapted type of neuron – a ‘nociceptive neuron’. To emphasise the point, scientists ascribe the theoretically crucial biological task of detecting noxious energy to sensory neurons. To understand this task you need to understand ‘noxious energy’ which, in turn, requires an understanding of the ‘damage threshold’. As a consequence of the ascription of a sensory function to pain, mainstream scientists are committed to sensory accuracy. In this context, sensory accuracy means the lowest nociceptive ‘stimulus threshold’ closely matches the damage threshold of tissue.
Sensory accuracy is a big problem for mainstream theory. In the above I have highlighted the difficulty posed by the variability of the damage threshold when tissue damage is present. A biological mechanism, the release of algogenic substances, changes the stimulus thresholds of sensory neurons but, I will explain in the next part of the tutorial, this mechanism does not solve the sensory accuracy problem.
The Pain Jam 