Dan Baumgardt, Senior Lecturer, School of Physiology, Pharmacology and Neuroscience, University of Bristol
11 February 2025
In the second world war, the physician Henry Beecher observed that some of his soldier patients, despite being injured on the battlefield, required no strong painkillers to manage their pain. In some cases, the injury was as severe as losing part of a limb.
A truly remarkable phenomenon had come into play – the effects of fear, stress and emotion on the brain had switched off their pain. But how does this work – and how can we use it to our advantage?
We all struggle with pain at times. The burning of indigestion, the wince of a scald from the kettle. The sharp stabbing of a sliced finger.
But despite its unpleasantness, pain has a critically important purpose, designed to protect the body rather than harm it. A fundamental concept to first understand is that you do not detect pain – it is a sensation. A sensation that your brain has created – from information it receives from the countless neurons (nerve cells) which supply your skin.
These specialised neurons are called nociceptors – they detect stimuli which are noxious, or potentially damaging to the body. This stimulation might range from a mechanical cut or crush injury, to extreme hot or cold temperatures.
So, if you touch a hot iron, or stand on a sharp nail, the correct reaction is to move your hand or foot away from it. The brain responds to pain by initiating muscle contractions in your arm or leg. In doing so, any further damage is averted.
The course of information, rushing along one neuron to another in a relay, is carried as electrical currents called action potentials. These begin at the skin, travel along nerve highways and into the spinal cord. When the information reaches the uppermost level of the brain – the cerebral cortex – a sensation of pain is generated.
Blocking pain signals
Many different factors can interfere with this transmission of information – we don’t perceive pain if the route to the cortex is blocked. Take the use of anaesthetics, for instance.
Local anaesthetics are injected directly into the skin to deactivate nociceptors (like lidocaine) - perhaps in A+E to perform stitches. Other agents induce a loss of consciousness – these are general anaesthetics, for more extensive surgical operations.
Pain is also a very variable experience. Commonly, we ask patients to quantify their pain by giving a value along a scale of nought to ten. What one person would consider a five out of ten pain, another might consider a seven – and another a two.
Some patients are born without the ability to sense pain – this rare condition is called congenital analgesia. You might think this confers an advantage, but the truth is quite the opposite. These individuals will be unaware of circumstances where their bodies are being damaged, and can end up sustaining more profound injuries, or missing them entirely and suffering the consequences.
How to trick your brain
What is more extraordinary is that we all possess an innate ability to control our pain levels. In fact, a natural painkiller is found deep within the nervous system itself.
The secret lies in a structure located in the very middle of your brain: the periaqueductal grey (PAG). This small, heart-shaped region contains neurons whose role is to alter incoming pain signals reaching the cerebral cortex. In doing so, it is able to dampen down any pain that would otherwise be experienced.
Let’s consider this in practice using the extreme example of the battlefield. This is an instance where sensing pain might actually prove more of a hindrance than of help. It might hamper a soldier’s ability to run, or assist comrades. In temporarily numbing the pain, the soldier becomes able to escape the dangerous environment and seek refuge.
But we encounter many examples of this ability coming into action in our everyday routines. Ever picked something in the kitchen that you suddenly realise is extremely hot? Sometimes that casserole dish or saucepan descends to the floor, but sometimes we are able to hold on just long enough to transfer it to the stove-top. This action may be underpinned by the PAG shutting off the sensation of clasping something too hot to handle, just long enough to prevent dropping it.
The substances which generate this effect are called enkephalins. They are produced in many different areas of the brain (including the PAG) and spinal cord, and may have similar actions to strong analgesics such as morphine. It has also been suggested that long term or chronic pain – which is persistent and not useful to the body – might arise as a result of abnormalities within this natural analgesic system.
This begs the question: how might you go about hacking your own nervous system to produce an analgesic effect?
There is growing evidence to suggest that the release of painkilling enkephalins can be enhanced in a variety of different ways. Exercise is one example – one of the reasons why prescribed exercise might be able to work wonders for aches and pains (backache for instance) instead of popping paracetamols.
Besides this, stressful situations, feeding and sex might also affect the activity of enkephalins and other related compounds.
So, how could we go about it? Take up strength or endurance training? Alleviate our stress? Good food? Good sex? While more work is needed to clarify a role for these options in pain management, their reward might be greater than we thought.
Pain remains a complex, poorly understood experience, but the future is bright. Only last month, the FDA approved the use of a new medication Journavx for managing acute pain.
Developing new painkilling treatments relies on the work of pain researchers to help unravel the intricate neuronal circuitry and function. There is no denying that this is going to be difficult task. But in considering the neuroscience of how our bodies generate and suppress pain, we can hope to understand how they can act as their own healers.
Dan Baumgardt does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.
This article is republished from The Conversation under a Creative Commons license.