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.
The Pain Jam 