Understanding Pain

“….the will is the string, its frustration or impediment the vibration 

of the string, knowledge the sounding-board, and pain the sound.”

‘On the Suffering of the World’

Arthur Schopenhauer


From the time of René Descartes in the mid-seventeenth century, western science and medicine have been greatly influenced by ‘dualistic’ theories of pain (that is, with clear divisions made between mental and physical experience) that have tended to emphasise the role of a specific injured body part communicating ‘pain signals’ to a specific ‘pain centre’ in the brain. Unfortunately, Descartes himself got into a big mess over this largely due to his central concern with soul. He failed sensibly to account for how physical and ethereal ‘substances’ could meaningfully correlate in the way he suggested. However, other ‘specificity’ theories (as they are known) flourished well into the twentieth century, describing the experience of pain as akin to a sense and functioning in the same way (or so we might suppose) as taste or smell. Still today, arguably, pain is regarded in the popular imagination as an essentially ‘bottom-up’ (that is, body-to-brain) process in which the brain is passive, instrumental. Under this view, any painful sensation relates to some stimulus or other that causes actual or potential bodily damage. 

Something of a revolution in pain began in the 1960s which has largely overturned Descartes’ legacy and continues to throw up new questions and discoveries about the nature of pain. In this post, I will describe in brief this change in perspective and one or two as yet unresolved problems that arise from it. This forms part of a paper soon – hopefully – to be published in which I will offering some direction as to how psychological therapists particularly (but not exclusively) can work effectively with people presenting with chronic pain. More about that later!

Pain as a response to threat

Though so-called specificity theories of pain make emotional sense – after all, it feels right to suggest that pain comes from the body – we now understand pain to be a ‘top-down’ affair, made not in the body but in the brain. There is no ‘pain centre’, however, no single part of the brain that is responsible for it. Different areas of the brain are constantly working together, making sense of all available information in order to evaluate whether pain would be advantageous at any given point. Pain makes sense as our brain’s principal protective response to credible evidence of threat: the truth is that our brain is something akin to a risk-averse, threat detecting machine.

So, what constitutes a threat of the sort that will lead to pain? Predictably, this question has no simple answer: pain is not just a matter of whether we have suffered a significant injury or not. In fact, what anyone finds threatening at any given time is very much a personal thing and depends greatly on context and on the innumerable differences between our lives. What is certainly important for us here is that each of us, in the very act of being ourselves, is formed of the relationships between different areas of a unique brain that, in our own particular circumstances, have repeatedly ‘fired’ together and ‘wired’ together, actively forming the myriad neurological pathways that, over the course of a lifetime, create a unique person with a unique set of experiences. What we find threatening – what leads our brain to create pain – will always be something to do with who we are and those formative influences that have helped to shape us. 

Nerves and pain 

Generally speaking, our nervous system sends not pain messages to our brain but what we might more helpfully think of as ‘danger’ messages – a process called nociception [noci – harm, injury, ception – understanding]. Nociceptive signals are very efficient at doing their job of constantly feeding back to our brain on the wear and tear experienced by our body moment by moment. Consequently, our central nervous system – essentially the spinal cord and brain – has had to become equally clever at giving selective attention to these messages by ‘gating off’ or inhibiting anything less urgent: it is advantageous, after all, that we don’t give as much of our time and emotional effort to the consequences of bumping into the edge of a table as we do to a life-threatening knife wound. When more intense nociceptive messages are strong enough to reach the brain and are corroborated either by sensory evidence – the sight of blood, the smell of smoke, the crying of a child – or by the memory of similar past circumstances and events, our brains will create protective pain.

Unfortunately, however, this kind of efficiency in nerves comes at a price. It is in the very nature of nociceptive fibres that they can become over-sensitive; too good at sending danger messages. This begins with the normal inflammatory process which results in the increased sensitivity of nerves at the site of an injury – known as peripheral sensitisation – a process that is inherently protective in that it stops us overusing or touching a damaged part of the body such as a twisted ankle. What is crucial for us here, however, is that rather than resolving once a tissue injury has healed, significantly raised levels of unhelpful and unnecessary nociceptive signals can go on being relayed to the brain in a way that is no longer protective. In fact, we know that not only the peripheral nervous system can become over-sensitised: the very neural pathways by which nociceptive danger signals travel through the spinal cord and up to the brain can themselves become ‘wound-up’ or ‘switched on’, a process known as central sensitisation. A significant increase in the sensitivity of the spinal cord can compromise the ‘gating’ process described above, leading nerve endings or synapses in the brain itself to become overstimulated. The loss of neural inhibition and the sensitisation of the spinal cord and brain are amongst the key factors contributing to the experience of chronic or persistent widespread pain.

You’d be right to be thinking at this point that talking about the sensitivity of nerves seems to take us right back to a more ‘bottom-up’ model of pain as created in the body. How do we reconcile the idea that pain results from an evaluative process in the brain – essentially, pain as having meaning – with pain as the result of increased neural sensitivity: one is qualitative where the other appears purely quantitative? In fact, this question points to the knot that different scientists are currently trying to untie. Crucially, however, we now know that central sensitisation can occur without nociception: the brain can get very ‘painy’ without incident or injury. This finding has led to some controversial descriptions of pain. For the purpose of what follows, we will state our own pragmatic position: the function of central sensitisation, however we explain it, is to reduce the threshold at which our very active brain will more readily conclude that making pain is advantageous.

Pain and stress

The fact that pain can lead to stress, anxiety and low mood is pretty obvious to anyone who has had even the slightest inkling of what it’s like living for a week with a toothache, let alone with a long term pain condition. It is not so obvious, perhaps, why our levels of stress should affect our experience of pain. The reason is that stress, like pain, is itself a response to threat: it is a warning signal that in the short term may say, ‘revise, revise, revise!’ if we are to have a hope of passing that exam. In the longer term, it may say, ‘Change your job; these hours are killing you!’. And, of course, the stress caused by pain says, in no uncertain terms, ‘What’s up with you?! – stop it hurting you idiot!’ When we can’t just kill the pain – and lasting, silver bullet, stake through the heart pain relief for chronic pain sufferers is not an option – the stress that should prompt us to action effectively turns against us; we get still more stressed by the lack of a solution and, when more stressed, more threatened, meaning that, even without any substantive change to tissue health, our perception of pain is likely to increase. And increase. And so on. The so-called ‘pain-stress’ cycle, as it is known, becomes largely self-maintaining. The undoing of Cartesian dualism as a model of pain is made concrete by the fact that without any intensification in the strength of nociceptive signals, the impact of stress can be to change the way parts of the brain that are central to pain evaluation actually function, effectively adding to the sensitivity of the whole process.

Pain perception

The crux of what I hope is conveyed in this post is that if we believe – as we did for centuries previously – that pain is in the body, we can make a distinction between pain as such and our perception of it. It would in fact be conceivable that a pain signal of a certain strength might get misread by our brain due to a fault of some kind. Equally, if we are generally frightened of pain, we might overreact, apparently making it worse. However, as we now know that our brain is not simply a more or less sophisticated pain-o-meter, that in fact pain is made in the brain, the possibility of misreading it disappears. We can no longer make a meaningful distinction between pain and the perception of pain: they are one and the same thing. It follows then that our fears and beliefs about our pain have the ability to make the pain actually feel worse, to make it more difficult to carry. This, in my view, is the foremost and necessary conclusion of what we’ve called the revolution in pain science.

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