But whilst damage to our bodies may eventually demand our attention through the experience of pain, this experience can be ignored, sublimated or delayed by the brain. Pain is a warning system, informing us that there is a threat to the safety of our bodies or even that damage has already occurred, but if experiencing pain and receiving this information is not immediately beneficial then the message relaying this information will be de-prioritized and sometimes ignored by the brain. We all know how crippling and all-consuming the experience of pain can be, and if it might delay, for example, our flight to safety, then it is not immediately helpful and could even be dangerous. The relationship between physical damage and the experience of pain can tell us a lot about the complexity of the biological pain alarm system and the processing of the information about damage, the route this message takes, and why, how and when it can be disrupted.

Whilst playing for Milan against Chievo on 14 March 2010, David Beckham ruptured his Achilles tendon in the eighty-ninth minute of the game. Video footage shows him turning sharply and trying to control the ball – the sharp turn is probably what caused the injury. He then starts to limp because his ankle will no longer flex and extend since he has now lost the use of his calf muscles that rely on being fixed to the ankle bones via the Achilles tendon. It appears that initially he does not realize he has injured himself – I imagine most professional sportspeople exist with a level of discomfort that would be abnormal to the rest of us and so the natural tendency would be to ignore the messages reaching his brain and carry on in the context of practising his profession. He tries again to run up to the ball to kick it but finds that he cannot perform this action – his progress is halted not by pain, as yet, but by loss of mechanical function. The tear to his Achilles tendon has already occurred moments before, and whilst the process by which information about this damage is converted to an electrical signal began at the moment of injury, it has not yet registered in his brain as pain.

When you sustain an injury, the traumatized tissue releases and attracts chemicals called inflammatory mediators. The aim of these substances is to try to heal the damaged tissue, but they also play a role in triggering the pain alarm. The release of chemicals such as hydrogen ions, potassium ions, bradykinins and prostaglandins stimulates the harm-sensing receptors in the tissues. The first step in the body’s complex pain alarm system, which we all possess (unless we are born with congenital hypoalgesia, which is a condition where people do not feel pain), is the conversion of damage to the body into an electrical signal. Throughout our bodies there exist receptors (which are like locks on doors) on free nerve endings called nociceptors – the prefix noci means harm or mischief in Greek – and these are harm-sensing receptors. Harm-sensing nerve endings are widely distributed in the skin, muscle, joints, organs and the lining of the brain, and are either covered with myelin, which is a fatty tissue, or are uncovered. Myelin-sheathed nerve endings (A delta fibres) conduct electricity faster than their thinner uncovered counterparts (C fibres); the faster signals from the A delta fibres make you instantly remove your hand from a hot object, whereas the slower fibres produce the sensation that teaches you not to do it again.

The human body can only be injured in three ways: mechanical trauma (such as gunshots, stabs, bumps and scrapes), chemical injury (a burn from an acid or an alkaline substance) and injury from extremes of temperature. All of these injuries result in the release of inflammatory mediators. Inflammation can also occur when the body’s immune system attacks itself or joints become inflamed. Nociceptors are of different classes and, like locks, they are all opened with different keys – intense pressure, temperatures greater than 40 to 45°C or less than 15°C, or chemicals released from injury and inflammation. In Beckham’s case, the damaged Achilles tendon releases substances including histamine, serotonin, bradykinin and hydrogen ions, which insert themselves into nociceptors, triggering an electrical impulse which communicates and codes for harm and damage, and begins its journey to the brain, where that message can be decoded.

The information that the body has been damaged first passes from the Achilles tendon to an area of the spinal cord called the dorsal horn and information is then passed into the substance of the spinal cord, which is an extension of the brain, and enables communication between the brain and the rest of the body. The dorsal horn is constantly receiving information both from the outer reaches of the body and from the brain via the spinal cord; it is like a bowl of soup whose flavour can be altered by inputs from the brain or from the peripheral nerves, rather than existing as a hardwired, fixed computer component. The face and neck are slightly different to the rest of the body, in that the nociceptive nerve endings meet in a structure called the trigeminal ganglion which projects to the brainstem that is located in the base of the brain.

Once the thin C fibres and fat A delta fibres mentioned above have conveyed information to the first and second layers of the dorsal horn, a chemical substance called glutamate is released from the dorsal horn nerves when the electrical signal generated from nociceptor activity reaches it and this opens doors within the spinal cord, sending a message to the brain about what has happened. The graver the injury, or the more times it is inflicted, the more keys are made available and the more doors are opened, resulting in more information being sent from the spinal cord to the brain – a phenomenon called wind-up, which contributes to the persistence of pain even when the injury has healed.

There are five superhighways of information ascending to the brain from the spinal cord – the spinothalamic tract (the ‘where is the problem’ pathway); the spinoreticular and spinomesencephalic tracts (triggering arousal, emotion, fight or flight instincts and activating motivation circuits in the brain which determine how we behave towards injury based on previous experience); and the cervicothalamic and spinohypothalamic pathways (controlling the regulation of hormones).

From the Achilles tendon this information rushes to the brain via these superhighways in the spinal cord and lights up different parts of the brain like the colours from a single firework which when ignited spreads across the night sky. The information travels to the area of the brain called the thalamus which is connected to the sensory part of the brain which deals with location and sensation (spinothalamic), as well as the areas which are responsible for sensing and coordinating emotion (spinohypothalamic), mediating the emotional components of pain. The survival and awareness areas of the brain are reached via the spinoreticular circuit, bringing into play the areas that facilitate an increase in heart rate, blood glucose and blood pressure to deal with whatever danger may be around. Connections are also made to the parts of the brain that deal with motivation. We are driven as humans by that which is necessary for survival – food, sleep, the avoidance of pain – and we are also driven by rewards which can be any experience that facilitates learning or results in pleasure; these motivation circuits develop early on and continue developing throughout our lives, determining how we behave. The damage signals also reach the parts of the brain that can release substances which cause pain relief (naturally occurring opioids and cannabinoids). Connections are made to the pathways that descend from the brain to the spinal cord and which are responsible for suppressing signals from the spinal cord, reducing the unpleasant information reaching the brain and thereby reducing the pain experienced. Pain is therefore always a sensory and an emotional experience, as these ‘superhighways’ connect to areas of the brain that involve both.

What is interesting when rewatching the footage of Beckham being injured is that initially there is no indication that he is in pain – he frowns, more confused than distressed, and continues to try to play. He eventually realizes that he cannot kick the ball and examines the area of his body that is not working properly. He knows where he has been injured because his brain has already received a message from the Achilles tendon which has registered in the part of the brain that deals with location when it comes to pain, but we do not yet see his outward expression of pain because the information is still being considered and evaluated.

What follows this assessment of the injured area is the realization of the injury and, more importantly, its meaning for him as an individual. This information is then processed through the parts of his brain that deal with emotion and context (the hypothalamus). I bet his initial thought was, ‘No World Cup. There goes my chance of captaining England.’ Once this information has been processed by his brain, we see him collapse under the weight of the implication of this injury. He lies on the ground distraught, holding his head in his hands. We see not only the expressions of pain but also the very visible experience of suffering. The sequence of events that we have witnessed, from the moment that he struggles to strike the ball to his collapse, is a powerful example of how pain and injury are not proportional to one another. It is only when an individual processes the injury in terms of attaching meaning to it that the expressions of suffering and pain are exhibited. In this way pain is a form of communication – it allows other people to see what the injury means to us as individuals and it has survival value in that our expression of pain will produce empathy and assistance.

Beckham sits on the bench with a towel over his head. The injury has not healed and therefore harm-sensing receptors are still being activated – nociception is ongoing. The information continues to reach the parts of his brain that were activated at the time of the injury, but he is no longer rolling about on the pitch; the experience of pain has been suppressed to a degree. This is caused by the activation of descending inhibitory pathways which project from the brain down to the spinal cord. The brain, therefore, can modulate the information coming up from the injured area and the pain experience is altered. The brain acts like a policeman controlling traffic, deciding how many of the cars coming from the Achilles tendon are allowed through. The brain also decides how much attention to pay to the individual drivers of these cars. The need for immediate attention is over for Beckham – the behaviours which he exhibited are no longer necessary, nor are they socially or psychologically acceptable. The game must go on and he must retire privately to decide on where he goes from this point in his life. This is the loneliness of the pain experience.

The descending inhibitory pathways which project from the brain are poorly understood. Functional magnetic resonance imaging (fMRI), which lights up parts of the brain in response to a painful stimulus, has been used to theorize about which areas of the brain are involved in suppressing pain. Parts of the emotional centre of the brain, the hypothalamus, which is responsible for appraising the sensory information, as well as the rostroventral medulla (part of the midbrain), are important for integrating these descending pathways to the spinal cord. Interestingly the same brain chemicals which we try to increase with medication when treating depression (serotonin and noradrenaline) are fundamental to the activation and functioning of these pathways. This is why individuals who are depressed often experience increased pain, because the lower levels of these chemical neurotransmitters are insufficient to activate the descending inhibitory pathways.

And so, we see that not all signals that are being sent from the Achilles tendon are being perceived in Beckham’s brain at the point of injury and in the immediate aftermath. Attention to the injury, emotional processing of the experience, expectation and thinking about the meaning of what has happened – these are all triggering return messages from the brain that regulate and control the information travelling from the injured area and moderate the consequent pain suffered.

I often use the example of David Beckham’s injured tendon when I explain to medical students the difference between tissue damage and pain. Initially he does not appear to be in pain; although of course we do not know that this is the case and can only surmise from the behaviour that he exhibits. He tries to continue to play. The information about the damage has already reached his brain but until he makes sense of what has gone wrong, we would not recognize his behaviour as that of exhibiting pain. This same situation, with regards to the mental processing of an injury, is why soldiers injured in battle are sometimes not found to complain significantly of pain even in the presence of horrific injuries such as amputations. The immediate concern of the individual is to get to safety and the brain can override the pain experience to facilitate this. It is only when soldiers reach a place of safety that an appraisal of the injury can be made. The injury results in the soldier having to leave the battlefield – a place of danger – and once this stress factor is removed the individual’s response to the injury similarly changes. In 1981, Ronald Reagan was shot in an attempted assassination. He recalled later that he only realized he had been shot in the chest when he felt and saw the blood seeping through his shirt in the limousine on the way to hospital.

The above examples of a delayed pain experience can be contrasted with those of people who are caught in fires, where immediate and severe pain is experienced. When you have been burnt in a civilian situation there is none of the modulating environment of a battlefield with its chaos or the distraction of being hastened to safety by Secret Service agents and nor, crucially, was there any expectation of possible injury when entering the arena and so the event is unexpected and thus deemed catastrophic by the victim. Burn injuries are also amongst the most painful given the degree of damage which is done and the widespread activation of harm-sensing receptors on nerve endings.

We all appreciate and understand the kind of pain described above, caused when tissues are broken, torn or damaged in some way; it is no different, perhaps, from the experience of primitive or ancient man, who understood the pain inflicted by an arrow, but failed to appreciate the pain from degenerative joints or infected, inflamed tissues. But as we have seen, injury and pain are not proportional, and the outcome of pain is dependent on more than just the degree of damage sustained – this can be harder to understand.

Pain as an experience is influenced by beliefs and expectations as well as psychological factors such as mood and resilience. An individual’s culture, genetics and innate ability to cope with adversity will all impact on their experience of pain. The rupture of an Achilles tendon on a squash court has very different implications to the same injury in a professional footballer who has aspirations of captaining a national side in a World Cup tournament; a soldier on the battlefield responds very differently to discomfort or injury than a member of the public who is injured at home, yet they both have the same internal chemistry.

The complexity of the psychological experience of pain is often best understood by looking at an individual’s reaction when they sustain an injury – their facial expressions, language and the sounds they make. But this needs to be considered alongside the physical processes taking place; the danger is that we might begin to consider the psychological experience as being separate from the pain pathways that I have described above. I talked about activation, for example, of the fight or flight system. We know that the release of adrenaline as a response to stress can cause an increase in muscle tension and the increase in muscle tension reduces blood flow (and therefore oxygen supply) to the muscle, which then releases bradykinin in response to being starved of oxygen; the bradykinin then activates more harm-sensing receptors. Anxiety and stress, therefore, which we would regard as psychological constructs, influence the pain experience on a biological basis. If a doctor is kind to you in a hospital when you are in pain, then that pain can be relieved to a degree even before the doctor has given you any pain relief, because kindness activates the descending inhibitory pathways. Similarly, whilst hostile social situations or hazardous environmental factors can cause the suppression of pain, as we saw in the instance of soldiers on a battlefield, in other environments these factors can actually aggravate the pain experience because, as we saw with adrenaline, stress influences the production of hormones, which activate parts of the brain that can either exacerbate or relieve the pain. The differing effects of psychosocial factors on an individual’s pain experience depend on how they are interpreted. There is, therefore, an integral relationship between psychological, social and environmental factors with tissue injury. This is why, when considering the experience of pain, a biopsychosocial model is used, which proposes that psychological and behavioural processes are mediated by the individual’s biology, rather than representing some esoteric force which descends from the ether – in other words, eventually it’s all down to chemistry.

As human beings we struggle with understanding how our behaviours and thoughts influence our biology via hormones and neurotransmitter chemicals. It is why individuals with mental health disorders are so marginalized and poorly understood and are therefore discriminated against, whilst we readily accept high blood pressure as a disease because it has a physiological explanation, even if most of us would never be able to outline how blood pressure functions within our bodies. Very few individuals understand that normal blood pressure is the product of the output of the heart multiplied by the resistance in ...