The Pain Jam

How to treat pain #3

Pain does not have a sensory function

In the previous part of this tutorial I set out the mainstream understanding of pain’s function: pain functions as the conscious awareness of a tissue damaging or threatening stimulus (in technical terms a ‘noxious stimulus’). In broader terms, the view of mainstream science is that pain has a sensory function. The claim that an experience has a sensory function comes with a commitment to sensory accuracy because inefficient biological systems tend to be refined or eliminated by evolutionary pressures. If an undeniably sensory experience like vision unreliably represented the world, then survival would be severely compromised. So the closeness of the correlation between pain and noxious energy is an important test of the truth of mainstream functional theory. In the third part of this tutorial I will examine this correlation, and conclude that the correlation is very weak indeed. For this reason, mainstream functional theory should be abandoned.

3.1 Preliminary comments – the evidence, and a distinction

My argument for the position that pain does not have a sensory function is strong because the evidence is that the correlation between pain and noxious energy is weak (for open access see Melzack and Wall’s 1996 book “The Challenge of Pain”; Lorimer Moseley’s 2007 paper, “Reconceptualising pain according to modern pain science”, is a typical example of an evidential review, but it is restricted access). Pain scientists accept this evidence, so they have powerful reason to draw the same functional conclusion as me. Yet the mainstream view persists. Perhaps scientists are unaware that they are committed to sensory accuracy, but I have no real explanation for the oversight and I have no intention of further speculation.

To recap, in part 2 the important distinction between the concepts ‘noxious energy’ and ‘noxious stimulus’ was discussed. In the scientific literature, this distinction is not clear because commentators often use ‘noxious stimulus’ to refer to noxious energy. This is a serious mistake. Noxious energy is energy at a bodily location (L) that is damaging or threatening to damage the tissue at L. A noxious stimulus is noxious energy at L that is being detected by a specifically adapted sensory neuron (i.e. a ‘nociceptive neuron’). Noxious energy exists in the meaningful sense that energy at a bodily location actually causes tissue damage. The metaphysical status of a noxious stimulus is far less certain. If noxious energy is not detected by sensory neurons, then there are no noxious stimuli:

A noxious stimulus exists if (and only if) sensory neurons are specifically adapted to detect noxious energy (i.e. if nociceptive neurons exist).

My use of ‘noxious energy’ and ‘noxious stimulus’ above and below reflects this important distinction.

3.2 Does pain correlate with noxious energy?

What is a correlation? A correlation refers to things that happen at the same time or that follow one another. A correlation does not mean causation. The fact that I usually see a particular person cycling past my house as I open my curtains in the morning does not imply a causal relationship between the cycling and the curtain opening. The best explanation for the cycling/curtain opening example concerns the respective morning routines of cyclist and observer; it has nothing to do with causation. The crucial point is that a strong correlation is consistent with causation. A weak correlation, if not entirely inconsistent, strongly suggests the absence of a causal relationship.

In this context, a strong correlation would mean that pain relates to noxious energy in three ways:

Pain is rarely experienced in the absence of noxious energy.
Energy rarely has a noxious effect in the absence of pain.
The intensity of pain usually, more or less, corresponds to the intensity of noxious energy.

It is widely accepted that pain fails on all three counts. Pain is often experienced in the absence of noxious energy; energy commonly has a noxious effect in the absence of pain; and the intensity of pain does not accurately represent the intensity of noxious energy. Mainstream pain treatment is presented in a way that suggests the weak correlation is confined to longstanding (i.e. ‘chronic’ pains), but it is also an obvious and normal aspect of the injury state.

In part 2 of this tutorial, I presented the variability of the damage threshold when tissue is damaged as a problem for mainstream functional theory. When tissue is damaged the intensity of energy required to cause (more) damage falls. In other words, intensities of energy that were not noxious in the undamaged state become noxious in the damaged state. So, given the requirement for sensory accuracy, the claim that pain has a sensory function requires a biological mechanism that not only lowers the thresholds of nociceptive neurons in the presence of tissue damage but also requires the matching of the lowest nociceptive stimulus threshold to the damage threshold. Scientists have established that algogenic (i.e. pain-promoting) substances released in the vicinity of damaged tissue lower the stimulus thresholds of sensory neurons. However, algogenic substance release is a crude mechanism that could not match, even moderately closely, stimulus thresholds with the damage threshold.

If the function of pain is to make us consciously aware of noxious energy then, normally, pain should be experienced only when energy is having a noxious effect (i.e. energy is damaging tissue – remember I am ignoring tissue-threatening energy for the sake of explanatory simplicity; see part 2, 2.2). In terms of thresholds, this means that the lowest stimulus threshold of nociceptive neurons at a particular bodily location (L) should be the same as the damage threshold of the tissues at L. But persuasive evidence that, in the presence of tissue damage, there is no match between these thresholds is provided by ordinary observation of the variability of pain. For example, when someone has an ankle ligament sprain (often referred to as a “twisted ankle”) it is very common for that person to feel a lot of pain when standing from sitting. But once they’ve tentatively moved around for a while the pain usually eases to a noticeable extent. In terms of the relationship between pain and the stimulus, this is evidence that there is often an inverse relationship between pain and the stimulus in the presence of injury. After the initial intense experience, cautious weight-bearing and movement (these constitute a mechanical stimulus) cause the pain to decrease in intensity and, in turn, this allows the person to bear more weight and move less cautiously. To be absolutely clear, for a time pain intensity decreases as stimulus intensity increases – hence the inverse relationship. Of course, this does not mean that pain will continue to decrease as stimulus intensity increases. If stimulus intensity continued to increase or remained constant for an extended period, then pain would almost certainly increase.

A subtle inverse relationship is often also evident in the chronic pain state; cautious movement causes pain, but repetition brings about an easing.

As the variability of the relationship between pain and noxious energy is a normal aspect of both periods of injury and chronic pain, it is a reasonable question when is it normal for pain to closely correlate with noxious energy. The answer is in a very limited set of circumstances. Crucially, from the perspective of mainstream pain theory, closer correlation is evident in the experimental setting. But correlation-supporting experiments themselves are limited in scope by the demands of experimental design. Specifically, the related reasons of reproducibility (where repetition of an experimental method is used to test the result of another experiment) and control (there are usually various variable strands to the object of a scientific enquiry; to draw a strong conclusion about one variable requires control of other variables), relevant pain experiments are usually conducted on undamaged skin using thermal or electrical stimuli.

Although, many of these experiments show a strong correlation between pain and noxious energy, their limitations are such that they can hardly be taken as powerful support for the mainstream theory that most acute pain (NB. acute pain is an episode of pain of relatively short duration) correlates with noxious energy, let alone that pain, as a whole, functions as the conscious awareness of noxious stimuli.

It is clear that mainstream functional theory fails to account for a very large proportion of naturally occurring pains. This proportion is where the inconsistency lies. The only plausible conclusion is that mainstream theory is incorrect: pain does not function as the conscious awareness of noxious stimuli. The obvious question is:

What is the function of pain?

I answer this question in the next part of the tutorial.

How to treat pain #2

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.

How to treat pain – a tutorial

It has been a long time since I published anything on here. I could give you many (poor) reasons, but I have, at least, made a decent start on the following project. I’ve found this very difficult. You may have realised I’ve a tendency to elaborate rather too much. In writing this tutorial, I’ve found this temptation almost irresistible. Needless to say the editing process has been long and hard for me. I hope to publish the subsequent parts in a timely manner. (The following two are written, but needless to say the editing process goes on.) I hope you find it interesting.

PART 1

Introduction – the relationship between function, cause, and treatment

This tutorial is intended for anyone with an interest in pain treatment, whether you are a theorist, a medical professional, or a layman wanting to better understand your own or someone else’s pain.

The watchword of any effective treatment approach is ‘understanding’:

If you do not have a proper understanding of pain in the general sense you are not equipped to adequately treat specific episodes of pain.

There is nothing controversial in this broad statement. No one could disagree that doing the right things will almost always ease pain, while doing the wrong things will exacerbate pain. This rather trivial comment is intended to emphasise the reason why education and understanding are central to effective treatment:

If you understand pain, then you are ideally placed to identify what is, and what is not, appropriate for specific episodes of pain.

The aim of this tutorial is to provide the educational material needed to establish this understanding.

The tutorial is divided into two sections. Each section is further divided into a number of parts with distinct themes. The first section of the tutorial concerns crucial background theory. In essence I set out to answer the question:

Why do we feel pain?

This question, which concerns the function of pain, is fundamental to all pain treatment. It is fundamental because establishing an effective way of approaching any specific pain depends on correct theory. Crucially, mainstream science is wrong about pain’s function. Consequently, the mainstream educational to pain treatment is not as effective as it should be.

The functional theory presented in the first section underpins the more practical content of the second section. It takes the answer to the functional question ‘Why do we feel pain?’ as a means of interpreting patterns of pain so that treatment can be individualised. In metaphorical terms, the second section teaches you how to understand what pain is telling you.

The rest of this introduction serves as a summary of the first section of the tutorial.

1.1 The relationship between pain and injury – the mainstream view

The question “Why do we feel pain” concerns the functional relationship between pain and injury. It is obvious that pain and injury are linked in some way because we feel pain far more frequently when we are injured. Commonly, it is believed that injury causes pain. The mistaken idea that pain functions to make us consciously aware of injury is derived from this causal understanding of the relationship between pain and injury. Although medical professionals may say things that tend to reinforce the mistaken common view, they do not really mean that injury is a direct cause of pain. Rather, they would say that pain is normally caused by noxious stimulation. In functional terms, the scientific mainstream believes:

Pain functions to make us consciously aware of noxious stimuli.

To highlight the subtle difference between the ordinary and mainstream scientific understandings of cause, a noxious stimulus is the thermal and mechanical energy that causes or could cause injury. A noxious stimulus is not the tissue damage itself. So, according to mainstream science, pain normally makes us aware of the causes or potential causes of injury

1.2 Orthodox functional theory and treatment

For the purpose of explanation it is helpful to think of pain treatment in terms of two strands that summarise all effective approaches to treatment:

S1 Avoid or minimise the negatives – where the negatives are the things that aggravate a specific pain.

S2 Do the positives – where the positives are the things that ease a specific pain.

In a sense, the distinction between these strands is artificial because the reduction of negatives can be seen as a positive thing to do. On this understanding, the things that fall under S1 are a sub-set of the things that fall under S2. I make the distinction because there seems a natural difference between a recommendation to do something and a recommendation not to do something.

In most cases, it is easy to establish, in general terms, what aggravates pain. For example, if bending to put on socks or pick something up from the floor gives rise to pain, then bending is an aggravating factor. From the mainstream functional standpoint, this particular example means that pain is making the person aware that bending is a noxious stimulus (i.e. bending is causing or could be causing tissue damage). The benefit of this awareness is that minimising bending will usually ease pain; where ‘easing’ means that it becomes less painful to bend (i.e. bending is less aggravating). In this way, the person in pain naturally bends more and, with time, bending becomes pain free. In mainstream terms, bending becomes less and less noxious. This is true improvement.

The problem is that, in this case, avoiding or minimising bending eases pain in another way: in the short term, there is less pain simply because the action causing pain is being avoided. Sometimes this leads a person into the psychological trap of thinking that pain causing activities are inherently harmful. In this case, the fact that pain is felt when bending underpins the false belief that bending is harmful. The trouble is that prolonged avoidance of activity tends to lead to prolonged episodes of and worsening pain, which in turn gives rise to the prohibition of still more activity. A vicious spiral.

Effective treatment is aimed at educating and reassuring. Mainstream education teaches that the stimulus is no longer noxious. Prolonged inactivity has brought about changes to the nervous system. Pain is being caused by a malfunction of the biological system that generates pain (the ‘pain system’). An explanation why some pains do not indicate harm or threat is intended to reassure that pain associated with the relaxation of self-imposed prohibition of activity does not mean damage. With careful planning, a gradual increase in activity tends to reduce the frequency and intensity of pain. A virtuous spiral.

In summary, the content of the mainstream educational approach is based on the theory that pain functions to make us consciously aware of noxious stimuli. Many episodes of pain are normal, in the sense that they are deemed to satisfy the sensory function of making us consciously aware of noxious stimuli. (Whether or not many “normal” pains actually correlate with noxious stimuli is open to question.) But most people who are referred on to mainstream educational programmes are deemed to be experiencing abnormal pains; pains that are not consistent with mainstream functional theory – the pain does not correlate with noxious stimulation.

Note the logical connection between functionally normal/abnormal pains and normal/abnormal pain system function. A pain that is satisfying its function is generated by normally functioning pain system; and a pain that is not satisfying its function is generated by an abnormally functioning pain system. So mainstream functional theory drives the mainstream understanding of abnormality. A pain is normal if (and only if) it satisfies the mainstream notion of function. A pain is abnormal if (and only if) it does not satisfy the mainstream notion of function.

1.3 Reasons to reject orthodox functional theory

There are many reasons to reject mainstream functional theory, and yet pain scientists are reluctant to do so. I have no idea why!

There are biological reasons, which I need not mention in this introduction. Another reason is that a noxious stimulus is a concept without any meaningful application; there are no actual noxious stimuli. (This is briefly discussed in part 3 of the tutorial, and argued in depth in a paper I will post at the same time as part 3.) Sensory inaccuracy, which I do mention here, is yet another reason.

The mainstream idea that pain functions to make us consciously aware of noxious energy is a sensory or perceptual concept. This concept is inconsistent with the overwhelming evidence that pain weakly correlates with noxious stimuli (i.e. pain is often experienced in the absence of a noxious stimulus and vice versa; and the intensity of pain does not reflect the intensity of the stimulus). Put another way, the evidence is that pain, conceived as a sensory experience, is commonly inaccurate. As the explanation for inaccuracy is pain system malfunction, pain system malfunction must also be commonplace. This contrasts starkly with experiences that are undeniably sensory in function, like vision, which are usually functionally accurate. Sensory inaccuracy and commonplace malfunction is inconsistent with evolutionary theory. Inefficient biological systems tend to be refined or eliminated by evolutionary pressures. So mainstream theory amounts to the claim that pain is beneficial, in the evolutionary sense, even though it often (perhaps most often) does not satisfy its function. It is a mistake to accept such a claim.

The only reasonable explanation for the frequency of so-called abnormal pains is that they are not abnormal. In which case, mainstream functional theory must be false. This has important implications for treatment.

1.4 An alternative understanding – pain has a motivational function

To a certain extent I have been unfair to mainstream pain scientists and theorists. The mainstream view is that pain has both sensory and motivational functions. However, scientists tend to focus on the former, and largely disregard the latter. If sensory function is ignored the occurrence of pain makes far more sense. On my alternative understanding:

Pain functions to motivate behaviour that avoids or minimises tissue damage.

Crucially, the pain system does not need to detect noxious energy to satisfy this motivational function:

The pain system does not detect noxious energy.

The implication being that the concept of noxious stimulation is nothing more than a myth. This explains the weak correlation between pain and noxious energy.

This does not mean that sensory input is unimportant. On the contrary, it is a critical aspect of pain system function. For practical purposes, sensory input is helpfully thought of in terms of information about what is being done (more appropriately, information about physical demand). A period of relative inactivity, whatever the reason for that inactivity, is a period when the provision of information is often insufficient for the pain system to respond accurately to demand. So the alternative explanation for the persistence of many episodes of pain, even though tissue is healing or healed, is that the pain system has not received sufficient information. This is a normal aspect of pain system function; it is not an abnormality.

1.5 Concluding remarks on treatment

Note the general nature of mainstream educational advice (in 1.2); it is not harmful to increase activity. Interpreted in terms of my alternative functional theory, the reason this general approach often brings improvement is that increased activity provides more information to the pain system. However, the error of mainstream theory is such that information cannot be individually fine-tuned. This means that some increases in activity are likely to be inappropriate and hinder improvement and some beneficial increases are missed altogether.

This tutorial is intended to provide you with the intellectual material you need to enable you to interpret patterns of pain so that behaviour can be individually modified to provide appropriate information to the pain system. In this way, you will be equipped to treat pain more effectively than any approach based on mainstream functional theory. This is the advantage of the educational approach I teach in this tutorial. My hope is that this introduction, at the very least, tempts you to read on.

Conceptual models of pain – a case of neglect

It’s been a long time since I posted anything on this blog. I had a good reason (past tense, of course). I began developing a course to help people treat or manage their own pain. A considerable project I intended to present as a series of episodes via this blog. But (there’s often a ‘but’) this project was abandoned, temporarily I want to add, in favour of other interests. In particular, the IASP (the International Association for the Study of Pain) published a new definition of pain. If you’ve read my previous posts you’ll know that the old (and original) definition was a hobbyhorse of mine. While the publication of a new definition wasn’t completely unexpected (the IASP released a revision for comment in 2019), its wording was surprising. One of the problems of the old version was its opacity, but the new version is no clearer than the old. I’ll blog about the new version in the near future. Thoughts about the new definition inspired me to resurrect another old hobbyhorse, the nociceptive system; the concept of a sensory system specifically adapted to discriminate noxious energy. I’ve now finished a paper (as yet unpublished) in which I argue there’s no such thing. Oh, and I’ve moved house. All of this is an excuse, but it’s also an introduction to the topic of this post (except the house bit) – the conceptual model that scientists use to frame experimental data (the definition of pain and the nociceptive system are aspects of this model).

A few days ago I listened to a podcast on the IASP’s Pain Research Forum website. Ostensibly, the discussion was about the encoding of sensory information; is this information preserved by specific neural pathways (by so-called ‘labelled lines’) or is it encoded in patterns of neurological activity. It’s widely accepted that this is not an either/or debate, that both are aspects of pain system neurology. But the contributors (all experts in the field) went further than this. One questioned whether the debate mattered. And all bemoaned existing theoretical models. It was quite anarchic and rather refreshing.

From the standpoint of someone who bats on about the inadequacy of theoretical models of pain (myself) the most telling comment was (to paraphrase) ‘Should we bin our theoretical models and just listen to the data.’ But we can’t just listen to the data. It would be like listening to a completely unfamiliar language. A conceptual framework is necessary to make sense of scientific data. It would be charitable to say that the contributors really mean that current theoretical models are inadequate, but the discussion suggested otherwise. Instead of urging conceptual review and revision, they seem to see the production of more data as the solution, but it isn’t a solution. To a certain extent this is understandable, data production is what they know best. But it is no excuse. While the contributors recognise the problem they don’t seem to see the obvious solution: more and better pain research. Unfortunately, unless conceptual research has greater prestige and attracts a level of funding that reflects its actual importance this situation is unlikely to change significantly. Ten years from now I can see the same contributors having a similar discussion and bemoaning the adequacy of theoretical models. Maybe then, as representatives of the pain science community generally, they’ll understand that more pain data is not a solution.

The paradox of pain

Pain has been called paradoxical for various reasons (for example, pain is a mental state and yet we have pains in parts of the body), but I have a particular paradox in mind; the contradiction between the positive impact pain has on our existence and our negative attitude towards pain. Now it may be that my positivity grates with some readers because pain can blight lives, but bear with me.

Years ago I came across a book with the arresting title “Pain: The Gift Nobody Wants” (by Paul Brand and Philip Yancey – later called “The Gift of Pain”), which neatly summarises our complex relationship with pain. On the one hand, pain fulfils the essential function of preventing or minimising injury; on the other hand, we don’t want to be in pain. These aspects of pain are intimately connected. Our dislike of pain motivates us to avoid or inhibit behaviour that causes pain, and in this way we avoid or inhibit behaviour that causes or could cause injury. Although negativity about pain is hard-wired in the experiential sense (we don’t want to be in pain), the functional contribution of pain is overwhelmingly advantageous. So why do we think negatively of pain?

To a certain extent the answer’s simply that we can’t see the wood for the trees – we can’t see pain’s advantage because we dislike being in pain. But many, including some experts, don’t even consider pain’s positive contribution to our lives. They see pain as an abnormality, as a problem in itself. Part of the reason for this is that pain research is heavily biased towards persistent maladaptive pain (often misleadingly called ‘chronic pain‘) – a prolonged episode of pain that’s not fulfilling its evolutionary function of preventing or minimising injury (i.e. it’s not adaptive, hence it’s maladaptive). The economic and personal (in terms of suffering) costs of maladaptive pain are huge, so the scientific and medical focus is understandable, but this does not excuse the widespread negativity that surrounds pain generally.

Pain: The Gift Nobody Wants focuses on people with leprosy; a disease that affects peripheral nerves making sufferers unable to experience pain. Not only are these people likely to suffer major injury, they are also vulnerable to repeated injury of the same part of the body. In this way, minor injuries can become serious enough to threaten survival. In order to prevent these problems an artificial pain system was developed. The prototype system utilised a light to warn the person to change behaviour. The premise that underpinned this prototype was that absence of pain amounts to a lack of awareness – the person injures herself because she doesn’t know she’s damaging tissue. But unfortunately this system was ineffective. You might think that, as rational creatures, knowledge of the (potentially) damaging consequences of an activity would be sufficient for someone to modify behaviour, but it was not. In many cases the desire to continue with whatever the person was doing outweighed any rationally driven motivation to cease.

Instead of utilising a warning light, the second artificial pain system delivered an electric shock to a body part unaffected by nerve damage so that activity likely to injure actually caused pain, but this too was largely unsuccessful. Clearly the pain generated by the artificial system motivated the person to behave in a way that eliminated the pain, but this could be done in one of two ways: by changing the activity causing the pain; or by disconnecting the pain system. It turned out that in many cases the desire to continue with some particular activity motivated people to disconnect the system despite the potential for injury.

What’s interesting is that the rational focus should be injury; after all, the consequences of injury can be very significant. And yet, the evidence is that the motivation to persist with an activity often outweighs any rationally generated motivation to stop. So an experience that warns without negative affect (i.e. unpleasantness) could not have evolved as a means of preventing or minimising injury for the simple reason that it does not work. The unpleasant nature of pain motivates directly and much more forcefully than rationality. The weakness of this means of preventing or minimising injury is that pain, not injury, is the central focus of our motivation; we want to get rid of pain. Hence we tend to see pain as the problem, not as the solution to the problem (of injury). Consequently, we behave in ways that mirror Brand and Yancey’s experiences with people with leprosy; when we take pain-killers our intention is to turn off the pain system. This is an extremely useful ability. It enables us to perform surgery without pain, and to ease or eliminate pain where appropriate (post-surgical or maladaptive pain, for example). Ironically, it’s easy to see the potential pitfalls of abuse of this ability when we reflect on the disconnection of Brand and Yancey’s artificial pain system, and yet we continue to see pain negatively and reach for the pain-killers. The trouble is that there’s a huge and very powerful pharmacological and treatment industry behind pain relief. This industry has a vested interest in reinforcing the natural tendency to view pain negatively, as something abnormal, as something undesirable that must be eliminated. Nothing could be further from the truth!

Defining pain – again!

A few days ago, when I was out walking, I ran into someone I’d met very briefly on holiday in Greece at the end of last year. It was one of those, ‘don’t I know you from somewhere’ meetings. The other day, without prompting, Pete began to talk about pain AND he perfectly quoted the International Association for the Study of Pain’s (the IASP’s) definition of pain. To say that I was surprised would be an understatement. It turns out that Pete’s professionally involved in pain; he’s an anaesthetist and he teaches pain to medical students. Feeling puckish, I couldn’t resist asking what the IASP’s definition means. To which he replied, “It’s not very clear is it; and it doesn’t apply to pathological pain [pain caused by damaged nerves or adaptive changes to the nervous system that have a harmful effect].” This statement, from someone who’s professionally involved in teaching pain, is a powerful illustration of the opacity of the IASP’s definition because it’s incorrect. But that’s not my point. It was his follow-up that struck me; “Of course, the IASP’s definition doesn’t matter because we all know what pain is.” My intuition is that most people would agree with Pete. It certainly explains the survival of the IASP’s wholly inadequate definition; most experts don’t care about the IASP’s definition because they think almost everyone knows what pain is. It’s the sensation you get when you bash an elbow, when you prick yourself on a thorn, get cramp or when you touch something hot.

What Pete means is that most of us are able to correctly identify whether an experiences is a pain or whether it’s not a pain. How do we do this? In short, we learn what pains feel like through, as the IASP put it, “experiences related to injury in early life” (2017 – see the IASP’s taxonomy of pain terms here). The way these experiences feel (their subjective character) gives us a template for pain. If an experience fits the template then the subject of that experience will judge that it’s a pain, and vice versa. The million dollar question is whether these judgements are reliable. This is a complex matter.

If pain were to be defined in accordance with Pete’s claim that we all know what pain is, then first-person judgements must be reliable. In fact, they’d be infallible: an experience is a pain because it has been judged (or would be judged) a pain by its subject who compares the fit of that experience with her pain template; or an experience is not a pain because it’s been judged (or would be judged) a non-pain by its subject who compares the fit of that experience with her pain template. While a different type of definition, which is not based on first-person judgement, does not imply unreliable first-person judgements it leaves open the question of whether first-person identification of an experience as pain (or a non-pain) is reliable.

My view is that scientific endorsement of the sort of subjective definition suggested by Pete’s ‘we all know what pain is’ would represent an endictment on the status of pain science. It’s true that pain science began as an investigation of the experiences we identify as pain using our pain template, but after many years of research and conceptual development we should expect the scientific definition of pain to deviate from this ordinary notion. I’m not going to go into my reasoning here, but I think that the IASP’s definition (“An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” – IASP, 2017 – see the IASP’s taxonomy of pain terms here – ) is an endorsement of the ordinary notion. This strongly suggests that pain science is still in its infancy. There’s certainly a great deal of work to be done!

The relationship between injury and pain

This entry’s intended to clear up the common misconception that the relationship between injury and pain is causal. Injury doesn’t cause pain. Well, not directly anyway. In my view, it’s best to think of the relationship as functional; injury is related to pain by the function of pain.

The relationship between injury and pain is not directly causal: I think most people have a confused understanding of the relationship between pain and injury. Most would, I think, say that injury causes pain. Meaning that pain is directly caused by damaged tissue. But if this were so, we should expect to feel pain constantly for the whole period of an injury; i.e. constantly (and I mean constantly) for weeks and months with the intensity of pain easing as the injured tissue heals. Yet most would, I think, see this as abnormal. Instead, they expect to feel pain at the moment when tissue becomes damaged and, perhaps, for a short time afterwards; and they expect pain to disappear when the injured body part is rested. Most also have an intuitive understanding that it’s normal to feel pain in the absence of injury; when you grab a hot pan-handle or your hair is pulled, for example. So almost everyone has an intuitive understanding inconsistent with the commonly stated belief that injury causes pain.

Surprisingly, scientific discourse is littered with much the same inconsistency. For example, the International Association for the Study of Pain (the ‘IASP’) state, “Many people report pain in the absence of tissue damage or any likely pathophysiological cause” and “if they report [pain] in the same way as pain caused by tissue damage…” But scientists also causally link pain with a noxious stimulus: “A stimulus that is damaging or threatens damage to normal tissues.” In this context, the word ‘stimulus’ refers to the mechanical and thermal energy detected by the sensory receptors involved in pain. And injury’s a tissue state (the state of being damaged); it’s not a type of energy.

While there’s no direct causal relationship between injury and pain. There are two ways that injury is an indirect cause of pain. First, a startling variety of biochemicals are released by and in the vicinity of damaged tissue. These biochemicals make sensory nerves more sensitive; the upshot being that the sensory nerves involved in pain react to lower intensities of mechanical and thermal energy. This is why you feel pain in response to lower intensities of energy when you have an injury; for example, when a bruise is quite gently pressed or you walk on a sprained ankle. To emphasise the point, this is indirect causation; the direct cause is the mechanical or thermal energy (that results from what you’re doing) at the site of sensitive nerves. The evidential reasons for rejecting direct causation are mentioned above: if injury were a direct cause of pain, then it’d be normal to feel pain constantly whenever you’re injured and it’d be abnormal to experience pain intermittently; and the sensory nerves involved in pain are directly stimulated by energy not damaged tissue.

The relationship between injury and pain is functional: There’s another (very) indirect way it might be stated that injury is causally related to pain. Injury compromises our ability to survive. This fact has lead to us evolving the capacity to feel pain. However, it isn’t helpful to think of this evolutionary relationship in causal terms; it’s far more informative to think of it functionally.

Scientists don’t often discuss the function of pain. Generally, the consensus is that pain functions as both a perceptual experience (as the conscious awareness of noxious stimuli) and a motivational experience (it motivates behaviour that prevents or minimises tissue damage). There are other schools of thought. Perhaps the most influential of these is the idea that pain has a homeostatic function. Specifically, pain functions to maintain bodily integrity. I’ve reservations about both these views, but these concerns are for another blog. My point here, has been to dispel the erroneous belief that injury is a direct cause of pain. The relationship between injury and pain is functional; it is not causal.

(A little more on the function of pain: The germ of the idea that pain functions to maintain bodily integrity can be found in Patrick Wall’s 1979 article “On the relation of injury to pain”, which inspired the title of this entry. In this paper, he argues that pain functions to promote healing not prevent injury. The more explicit notion that pain is a homeostatic emotion is to be found in A.D. Craig’s 2002 paper, “How do you feel? Interoception, the sense of the physiological condition of the body”. Unfortunately neither paper is open access. If you have institutional access you can find these papers here: Wall and Craig. Other accounts, by scientists, that are specific to pain’s function are difficult to find. Most references to function are to be found in scientific literature with another focus, but I’ll put my neck on the line and claim that, largely, these accounts conceive pain as a sensory (i.e. perceptual) experience. For example, Woolf and Ma state that pain functions as the conscious awareness of a noxious stimulus – this article is not open access, either, but here’s the link: Woolf and Ma. Although this may appear inconsistent with the view that pain motivates behaviour that prevents or minimises injury, it is not. Presumably the idea is that conscious awareness of a noxious stimulus fulfils a critical role in such motivation. By contrast, philosophers have plenty to say about pain’s function. The majority, under a variety of closely related but subtly distinct theories, tow the scientifically endorsed view that pain has a perceptual function. A recently published paper by Laurenz Casser challenges this view. I mention this paper specifically because it is very recent, well argued and provides strong reasons to reject the position that pain has a perceptual function. It’s available here, if you have institutional access: Casser.)

Pain is not suffering, and suffering is not pain

At an inter-disciplinary conference on “pain” several years ago, I struggled to make sense of the first-couple of presentations because the presenters used the words ‘pain’and ‘suffering’ interchangeably. Of course, it’s ordinary linguistic practice to use the word ‘pain’ (and synonyms for pain like ‘hurt’, ‘ache’, and ‘painful’) to refer to suffering. It’s normal to say such things as: “Her back pain’s preventing her from working”; “Losing that job has caused me real pain; “My knee hurts”; “He’s been hurting since she left him”; “This cut’s really painful”; “His death was so painful for me”. But it soon became clear me this wasn’t just a confusing use of terms, it reflected a blurring of the concepts of pain and suffering. In effect, these experts were saying that either some pains are a type of suffering or suffering is a type of pain. This is a mistake. Pain is not synonymous with suffering. The word ‘pain’ has two different meanings (i.e. it’s a homonym); it refers to distinct concepts.

Once experts start making mistakes those mistakes creep insidiously, via the media, into the general population. (This isn’t just an idle concern; in the media some experts and prominent commentators do talk about pain and suffering as though they’re more or less the same thing.) Why does this matter? My worry is that it’s elevating the psychological impact of pain. Someone who thinks that they’ll suffer if they’re in pain is likely to be anxious about both their current pains and the chances of future pain, and anxiety has the capacity (via well established biological mechanisms) to make pain worse.

The distinction between the concepts pain and suffering is marked by the intransitivity of the concept of pain, and the transitivity of the concept of suffering. It’s easier to understand the intransitive/transitive distinction if I explain transitivity first. When I’m suffering I don’t just suffer, I’m suffering something. If I say “I’m suffering”, the natural response is to ask, “What are you suffering?”. As the concept of suffering can’t be abstracted from its cause (i.e. the thing being suffered – a bereavement or chronic back pain, say), suffering is a transitive experience. By contrast, while all pains have a cause, the concept of pain is self-contained; it can be abstracted from cause. When I’m in pain the pain itself is my immediate focus. I might report this by saying “I’m in pain.” Nothing need be added to such a report. Pain is an intransitive concept.

The independence of the concept of pain is also evident in the fact that it’s perfectly consistent for me to talk of the pain I got when I touched something very hot and to deny suffering. However, the reverse claim’s not quite so straightforward because of the dual meanings of the word ‘pain’. Does it make sense to say, “I’m suffering the loss of my job, but I’m not feeling pain”?

The terms ‘physical pain’ and ‘psychological pain’ (or ‘mental pain’) are sometimes used to make sense of the meaning of ‘pain’ in statements like the one above. If I’m suffering the loss of a job, I must be experiencing psychological pain, because suffering something is psychological pain. In which case, my denial that I’m feeling pain refers to physical pain not psychological pain. I am stating that I’m experiencing psychological pain; I’m experiencing psychological, not physical, pain because I’ve lost my job. To add to the terminological complexity, psychological pain (i.e. suffering or transitive pain) can be causally related to physical pain (i.e. pain or intransitive pain). Likewise, physical pain can cause suffering.

You may well be confused by all of this. My view is that ‘physical pain’ and ‘psychological pain’ are unhelpful terms because they makes it seem as though pain and suffering are experiences of the same type. But they’re not experiences of the same type. The pain of touching something hot, of cramp, of a pin-prick doesn’t feel anything like the suffering of bereavement, of divorce, of bankruptcy. So pain is not suffering or even a type of suffering, and suffering is not pain or a type of pain.

Additionally, these terms suggest a misleading dualism. Both pain and suffering are psychological in the sense that they’re experiential mental states. And both are physical in the sense that they can, in principle, be explained in biological terms. (I’ve used an ‘in principle clause‘ because our current biological understanding of experiential consciousness is not developed enough to explain the relationship between mental and biological states.) For these reason, the terms ‘pain’ and ‘suffering’ are better than ‘physical pain’ and ‘psychological pain’, despite the potential confusion.

There’s no solution to this problem. The language of pain is also the language of suffering. My message is simple, don’t be mislead by the dual use of this language or ill-informed commentary in the media. Pain and suffering are distinct experiences, which is why we have distinct concepts of pain and suffering.

The importance of conceptual clarity – defining pain

This blog is closely related to my previous blog – “Stuart Derbyshire on foetal pain”. In that blog I reported that Stuart now rejects his former view that foetuses and early stage infants can’t feel pain because of a change in his theoretical position not because new evidence had emerged. This was intended to highlight the importance of theories and concepts. My target here is clarity; ambiguous concepts can have significant consequences.

Although I didn’t mention it in my previous blog, Stuart takes it that the International Association for the Study of Pain’s (the IASP’s) definition of pain requires higher-order mental capacities. In short, the idea that the development of the self is required for pain experience (see my previous blog for a bit more explanation of the ‘higher-order theory of pain‘). The IASP is so highly regarded that their understanding of what is required for pain really matters. (Here’s the link to the IASP’s taxonomy of pain terms.)

I’m pretty sure that Stuart’s misinterpreting the IASP’s definition (I’ll explain why in a moment), but for now let’s pretend that he’s right. This would mean that the IASP is sanctioning the theory that higher-order mental capacity is required for pain. Therefore, any living thing lacking this capacity wouldn’t be able to experience pain. So, according to pain science, foetuses, the new-born and many non-human species of animal wouldn’t feel pain. From this you can see that the mainstream adoption of a particular theory can have very important practical and moral consequences; foetuses, early stage infants, and non-human animals might be denied anaesthesia and analgaesia.

The worry that the IASP’s definition amounts to the official sanction of a higher-order theory of pain fuels a debate that still simmers today. (This debate was sparked by Anand and Craig’s 1996 paper, “New perspectives on the definition of pain” – unfortunately this paper is not open access.) But these concerns can be put down to a misreading of the IASP’s ambiguously worded definition: pain is “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”

What is meant by “associated with actual or potential tissue damage…” and “described in terms of…” is far from clear. Although there’s an explanatory note that accompanies the definition in the IASP’s taxonomy, it’s not very helpful. Over the years I’ve thought quite a lot about the definition and note. The ‘association’ and ‘description’ might be interpreted as requiring higher-order mental capacities (to associate and to describe), but I’ve come to think that the definition means this: pain is

Either an unpleasant sensory and emotional experience caused by actual or potential tissue damage,
Or an unpleasant sensory and emotional experience that feels just like an unpleasant sensory and emotional experience caused by actual or potential tissue damage.

I’m not saying that 1 and 2 are either clear or satisfactory as a definition. What I’m saying is that from the definition and note (and plenty of reading between the lines) it looks as though the IASP (and by extension mainstream pain science) intend something like 1 and 2. And 1 and 2 do not require higher-order mental capacity for pain. So the IASP’s definition does not exclude the possibility that animals lacking this capacity can feel pain.

My understanding is supported by a reformulated definition that was recently proposed (but not yet, as far as I’m aware, ratified) by the IASP’s taxonomy committee: pain is “An aversive sensory and emotional experience typically caused by, or resembling that caused by, actual or potential tissue injury“.

In my view, this reformulation would be unsatisfactory for several reasons (lack of clarity being one reason), but I’ll wait to see if it’s ratified before further comment. The point of this and my previous blog has been to illustrate the importance of concepts and theories. Broadly speaking, good science requires clear and coherent concepts and theories to frame experimental design and data. The evidence I’ll present over time shows that pain science has favoured the latter at the cost of the former.

Stuart Derbyshire on foetal pain

I’m interested to read that Stuart Derbyshire has changed his opinion on foetal pain. This is important because Stuart, who is associate professor of psychology at the National University of Singapore, has been and is a prominent researcher and commentator on foetal pain. His view was that foetuses and early stage infants can’t experience pain. Now he believes that foetuses may be able to feel pain as early as 12 weeks after gestation.

Of course, Stuart’s u-turn is interesting because it could have moral and practical impact, but it’s also interesting because it demonstrates the crucial role that theoretical models play in the interpretation of scientific evidence. In short, his argument that foetuses can’t feel pain went like this:

The evidence is that the cortex, which is part of the brain, is not mature until some weeks after birth.
A mature cortex is needed for anyone to be conscious of sensations like pain.
Therefore, foetuses and early stage infants can’t feel pain.

The focus of Stuart’s u-turn is (2), which needs a little explanation. It’s natural to say “I’m feeling pain”, or “There’s a pain in my leg”. Sentences or thoughts like this suggest a distinction between the I (the self) and the pain; I am experiencing this pain. This distinction is the basis of ‘higher-order theories of consciousness‘ (there are plenty of variations). The idea is that there’s no experience without someone (an I) to have the experience. As pains are experiences, there’s no pain unless the nervous system is sufficiently developed to support I (the self). In effect, a higher-order theory makes I part of (i.e. a constituent of) the experience. Stuart’s conclusion (3) that foetuses and early stage infants can’t feel pain was grounded in the evidence that the cortex isn’t mature enough to support I until a few weeks after birth (1), and his acceptance of a higher-order theory of pain (and other experiences)(2).

Stuart still believes that the cortex isn’t sufficiently developed to support I until the early stage infant is a few weeks old, but he now rejects the higher-order theory that I is a constituent of experiences like pain (2). (His rejection isn’t surprising, because a higher-order theory of experience is problematic for many reasons. Here’s a couple of reasons: it strongly suggests that most animal species are not conscious, which is implausible; and it’s difficult to explain how a higher-order mental state could develop before primitive states like pains, visual experiences, etc..) Instead, he distinguishes between the recognition that we’re having an experience (this is a higher-order mental state directed at a primitive mental state) and the experience itself (the primitive mental state – in this case, the pain). And, in his opinion, the foetal nervous system may be sufficiently developed to support experiences (including pain) as early as 12 weeks after gestation.

Although this is conceptually challenging stuff, in essence it illustrates why theories and concepts are so important. Stuart’s view on foetal and neonatal pain has changed because his overarching theory of experiential consciousness has changed; not because there’s new evidence of earlier maturation of the cortex.

If you want to read more, papers reflecting Stuart Derbyshire’s former and current views on foetal pain can be found here:

You can also find on-line explanations of higher-order theories of consciousness in the Stanford Encyclopaedia of Philosophy. The explanation in the ‘Consciousness’ entry here is more straightforward than the ‘Higher-Order Theories of Consciousness’ entry here but both are difficult for the uninitiated. I don’t think the Wikipedia entry is at all helpful because it uses technical terms without any explanation.