Oxford. Lauren Heathcote: The reasons you feel pain are much less straightforward than you may realise. Oxford researcher Lauren Heathcote probes the mystery. When I was fifteen, the pain started. At first it was mild, but soon there were constant shooting pains down my left leg. The MRI results were clear: a tumour in my pelvis. A big one. And it was pressing on my sciatic nerve. After a year of chemo and radiotherapy, the tumour shrunk and the pain went away.
A basic understanding of pain is that it tells us something’s wrong. You might think, and understandably so, that pain is the direct outcome of tissue damage. If I cut my finger, it hurts. If I cut it more, it hurts more. Right? Wrong. Contrary to popular belief, pain is not always a good indication of tissue damage. Pain is, in fact, a conscious output of the brain when an organism perceives tissue to be under threat. The key word here is perceives. It may perceive threat even when there is none. And it may ignore threat even when the threat is very real.
Our first clues came in the 1960s, when a Canadian researcher named Ronald Melzack, and an Oxford alum, Patrick Wall, conducted a series of animal experiments. They showed that rats displayed wildly different levels of pain behaviour but with the same level of tissue damage. That was clue number one.
Then they tested the nociceptors — free nerve endings all over (and inside) our bodies. These were, at least until the 60s, revered as the body’s ‘pain receptors’. Nociceptors are now better understood as the body’s danger detectors, sensing potential harm in the form of mechanical (pressure), thermal and chemical stimuli on the skin and inside the body. Melzack and Wall found that the level of nociception did not explain the rats’ level of pain behaviour. That was clue number two.
So for the rats, pain behaviour did not provide an accurate measure of tissue damage. And it soon became clear that the same is true for the feeling of pain in humans. Of course, anecdotal evidence has been providing clues for centuries. Think of the injured soldier, who feels no pain but keeps fighting. Think of the rugby player, who discovers his broken ankle only after the crowd has gone home. Clearly, in these situations, there is tissue damage. There is nociception — neural signalling of danger. But there is no pain.
In controlled laboratory settings, using healthy, normal volunteers — although (as leading researcher Lorimer Moseley has pointed out) just how ‘normal’ someone is who volunteers to be in a pain study is a reasonable question! — scientists have conducted experiments in which they simultaneously record activity in nociceptors and pain ratings. The evidence, once again, is that there is no straightforward relationship between tissue damage and pain.
So what does account for our feelings of pain? And why does the brain get it so wrong so often? In fact, the brain is actually doing something quite clever: using all of the available information to make a decision about the amount of threat to the tissues. This includes information not only from the nociceptors, but also from our other senses. And from data already stored within the brain itself.
In one study led by Lorimer Moseley at Oxford in 2007, a very cold piece of metal was placed on the back of volunteers’ hands—so cold that that it was likely to feel somewhat painful. At the same time, they were shown either a red or a blue light, but were told nothing about the light or its meaning. Amazingly, the volunteers reported more unpleasant and intense pain when they saw the red light than the blue light. This is because the brain used the information that red is a danger signal, and so produced a stronger danger signal of its own: more pain.
At fMRIB, the Oxford centre for functional magnetic resonance imaging of the brain, scientists are investigating how other types of information affect pain. Intriguingly, in a groundbreaking study just last week, the team identified for the first time a brain region that is seemingly pain-specific. However, this brain area is highly connected to other brain systems involved in memory and emotions such as fear and anxiety. And these systems talk to each other to decide how much pain to produce. So if you’re feeling anxious about having an injection, your brain will use this information as an indication of danger, and it will create more pain.
are also now beginning to understand what happens when pain persists.
Around one in ten people suffer from chronic pain, a condition that has
received recent media attention from Jennifer Aniston’s new movie Cake.
We now know that chronic pain disorders are caused by changes in the
brain and central nervous system. As pain persists, the neural system
dedicated to pain processing becomes increasingly sensitized, which
means that the relationship between pain and the state of the tissues
becomes weaker and less predictable. For these patients, pain is not a
symptom of another disorder; pain is the disorder. But this doesn’t mean that the pain isn’t real. Remember, all pain is created by the brain. No brain, no pain.
And if you need more convincing that chronic pain isn’t caused by weak, ageing tissues, children get it too. My personal experience with pain has led me to specialise in researching the role of the brain and mind in children’s experience of pain. Alongside clinicians at the Nuffield Orthopaedic Centre here in Oxford, and thanks to a fellowship grant from the UK charity Action Medical Research, my supervisors and I are developing new interventions for young people with chronic pain. These interventions are based on our understanding of the psychology and neuroscience of pain, and are designed to help change how the brain processes cues for pain.
It’s been said that pain is weakness leaving the body. But pain isn’t a weakness, it’s your brain trying to protect your body, and using every piece of information to do so. And this is a pretty amazing feat for a 1.4kg spongy thing inside your head, even if it does sometimes get it wrong.