Overview: An illuminating, authoritative, and in-depth examination of the fascinating science behind pain and the complexities of its treatment—from one of the internationally leading doctors in pain management.
Pain is a universal human experience, but we understand very little about the mechanics behind it. We hurt ourselves, we feel pain, we seek help from a professional or learn to avoid certain behaviors that cause pain. But the story of what goes on in our body is far from simple. Even medical practitioners themselves often fail to grasp the complexities between our minds and bodies and how they interact when dealing with pain stimulus. Throughout history we’ve tried to prevent and mediate the effects of pain—which has only resulted in a highly medicated population and a booming opiates industry.
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| An Anatomy of Pain How the Body and the Mind Experience and Endure Physical Suffering by Abdul-Ghaaliq Lalkhen Book |
An Anatomy of Pain How the Body and the Mind Experience and Endure Physical Suffering by Abdul-Ghaaliq Lalkhen Book Read Online Chapter One
You may have purchased this book to read while on vacation somewhere, as you bask in sunshine. Perhaps you are being tortured or delighted by the excited screams of children or feeling gentle breezes blowing from the sea, while the smell of sunscreen permeates the air. Your swimsuit may be slightly damp from being in the pool. Regardless of the sounds, smells, and temperatures you are exposed to, these sensations are all quite easy to tune out so they become background noise. However, if you were to be bitten by a mosquito or an exposed part of your body started to object to the strong sunlight, this experience would demand your attention and it would take a great deal of conscious effort to ignore. This is the universal experience of pain. Physiologists refer to pain as “aversive at threshold,” which means that it cannot be ignored or subdued easily. By its very nature it demands attention, and this is as true today, as you sit languishing idly around a swimming pool, as it was when we were a primitive species fighting for survival in a harsh and untamed world.
But while damage to our body 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 body 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.
While playing for Milan against Chievo on March 14, 2010, the soccer star 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, which 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 athletes exist with a level of discomfort that would be abnormal to the rest of us, and so Beckham’s natural tendency would be to ignore the messages reaching his brain and carry on in the context of practicing 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 occurred moments before, and while 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 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, 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 harm-sensing receptors (which are like locks on doors) on free nerve endings called nociceptors; the prefix noci means “harm” or “mischief” in Greek. 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 fibers) conduct electricity faster than their thinner, uncovered counterparts (C fibers); the faster signals from the A delta fibers make you instantly remove your hand from a hot object, whereas the slower fibers produce the sensation that teaches you not to touch the hot object again.
The human body can be injured in only three ways: by 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, are opened with different keys: intense pressure, temperatures greater than 104 to 113°F or less than 59°F, or chemicals released from injury and inflammation. In Beckham’s case, the damaged Achilles tendon released histamine, serotonin, bradykinin, hydrogen ions, and other substances that insert themselves into nociceptors, triggering an electrical impulse that communicates and codes for harm and damage and begins its journey to the brain, where that message can be decoded.
The information that his body had been damaged first passed from Beckham’s Achilles tendon to an area of the spinal cord called the dorsal horn; the information 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 flavor 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 from 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 fibers and fat A delta fibers 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. 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 that determine how we behave toward injury based on previous experience), and the cervicothalamic and spinohypothalamic pathways (controlling the regulation of hormones).
From Beckham’s Achilles tendon this information rushed to the brain via these superhighways in the spinal cord and lit up different parts of his brain like the colors from a single firework that spread across the night sky. The information traveled to the area of the brain called the thalamus, which is connected to the sensory part of the brain that deals with location and sensation (spinothalamic), as well as the areas 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 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 that cause pain relief (naturally occurring opioids and cannabinoids). And connections are made to the pathways that descend from the brain to the spinal cord and are responsible for suppressing signals from the spinal cord, reducing the unpleasant information reaching the brain and thereby reducing the pain we experience. 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 watching footage of Beckham being injured is that initially there is no indication that he is in pain—he simply 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 his Achilles tendon, which has registered in the part of the brain that deals with pain location, but we do not yet see his outward expression of pain because the information is still being considered and evaluated.
What follows his assessment of the injured area is his realization of the injury and, more important, its meaning for him as an individual. This information is processed through the parts of his brain that deal with emotion and context (the hypothalamus). I’ll 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 he struggles to kick the ball to his collapse, is a powerful example of how pain and injury are not proportional to one another. It is only when we process the injury by attaching meaning to it that we express suffering and pain. 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 field; the experience of pain has been suppressed to a degree. This is caused by the activation of descending inhibitory pathways that project from the brain down to the spinal cord. The brain can modulate the information coming up from the injured area, and the pain experience is altered. The brain acts like a police officer controlling traffic, deciding how many of the cars coming from Achilles Avenue are to be 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 behaviors 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 where he goes from this point in his life. This is the loneliness of the pain experience.
The descending inhibitory pathways that 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 center 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 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: 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 his 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 traveling from the injured area and moderate the consequent pain suffered.
I often use the example of 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 behavior 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 behavior as that of exhibiting pain. This same situation, the mental processing of an injury, is why soldiers injured in battle sometimes do not complain significantly of pain even in the presence of horrific injuries such as amputations. Their immediate concern 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 they make an appraisal of their injury. In 1981 President Ronald Reagan was shot in the chest in an attempted assassination. He recalled later that he realized he had been shot only when he felt and saw the blood seeping through his shirt in the limousine on the way to hospital.
These examples of a delayed pain experience can be contrasted with those of people who are caught in a fire. A fire has none of the modulating environment of a battlefield, with its chaos, or the distraction of being hastened to safety by Secret Service agents. Nor, crucially, does the person about to be burned expect the injury. Because the fire is a surprise and the injury unanticipated, the victim deems it catastrophic and experiences immediate and severe pain. Burn injuries are among the most painful given the degree of damage that is done and the widespread activation of harm-sensing receptors on nerve endings.
We all appreciate and understand the kind of pain I have described, caused when tissues are broken, torn, or damaged in some way; it is no different, perhaps, from the experience of primitive or ancient humans, 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 impact their experience of pain. The rupture of an Achilles tendon in a weekend squash player has very different implications from the same injury in a professional soccer player who has aspirations of captaining a national team in a World Cup tournament; a soldier on the battlefield responds very differently to discomfort 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 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 I have described. 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 that 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 when you are in pain, that pain may be relieved to a degree even before the doctor has given you any pain medicine, because kindness activates the descending inhibitory pathways. Similarly, while hostile social situations or hazardous environmental factors can cause the suppression of pain, as they do for 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 an integral relationship between psychological, social, and environmental factors and tissue injury. This is why, when considering the experience of pain, we use a biopsychosocial model, which proposes that psychological and behavioral processes are mediated by the individual’s biology, rather than representing some esoteric force that descends from the ether. In other words, eventually it’s all about chemistry.
As human beings we struggle to understand how our behaviors and thoughts influence our biology via hormones and neurotransmitter chemicals. This is why individuals with mental health disorders are so marginalized and poorly understood and are therefore discriminated against, while 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 resistance in the blood vessels and that abnormal blood pressure is a result of dysfunction of these blood vessels. We would not respond to somebody with high blood pressure by telling them to calm down or relax their blood vessels. Unfortunately, patients who present with pain that we consider to be in excess of what we would expect, or who have lowered mood, are often told to just get on with it and stop being histrionic.
Depression and anxiety play a role in the experience and report of pain. Catastrophizing is a psychological construct that consists of excessive rumination, magnification, and helplessness in the face of adversity and involves extreme negative thoughts about one’s plight. A higher level of catastrophizing, and consequently feeling a lower sense of control, is an important predictor that a patient will experience severe acute pain or develop chronic pain, when pain persists beyond what would be medically expected. Catastrophizing may be thought of as an exaggerated negative pattern of thinking during actual or anticipated painful experiences. Where patients catastrophize to a high degree they experience greater levels of pain and emotional distress. This abnormal pattern of thinking can have a significant biological impact, as it can increase pain signals and may result in increased sensitivity of the pain alarm, potentially leading to its permanent activation even after the once-damaged tissues have healed and resulting in progression from acute to chronic pain.
Chronic pain can in part be due to the development of pain-related fear, when patients adopt an approach to managing persistent pain by trying to avoid activities that might cause an increase in pain. Patients who have undergone surgery or experienced trauma and who have high levels of catastrophizing, for example, may find it difficult to rehabilitate because of this psychological construct. Their way of coping with pain is to avoid movement; this may have consequences such as the development of deep vein thrombosis when they remain in bed and the blood in their legs pools like stagnant water, as well as lung infections when they fail to cough or breathe deeply following surgery. These patients are also more likely to use higher doses of pain-relief medication.
Preoperative anxiety is one of the most consistent and predictable risk factors for the severity of postoperative pain. One of the key messages that I communicate to trainee doctors who assess patients prior to surgery is to never tell anybody that they will have no pain following surgery. I tell them to explain to the patient that if zero equals no pain and 10 is the worst pain imaginable, then at best we can probably get their pain down to 4 following the operation. If patients have this 4/10 construct in their heads when they wake up and assess the sensory information reaching their brain, it may allow them to cope better with the postoperative pain. If you tell them they will feel no pain when they wake up, then any unpleasant sensory information will be appraised in a catastrophic manner.
The importance of this approach is often emphasized to me when I look after patients who have had a laparotomy, which involves cutting through all of the abdominal muscles and tissues to get to the bowels. The incision is often four to six inches long and can extend from above the pubic bone to just below the chest. We use epidural pain relief for these operations; a catheter is threaded via a hollow needle into the epidural space, which lies just above the spinal cord, and the infused local anesthetic bathes the nerves as they leave the spine. This technique usually provides excellent pain relief for what is a massive traumatic incision. These operations also require patients to have a plastic breathing tube in their throat for a prolonged period and also to have a plastic drip put into one of their neck veins. I am always amazed when patients complain bitterly of the tube in their neck and a sore throat, and are almost unmanageable as a consequence, but don’t mind the six-inch laparotomy incision. The anesthesiologist’s preoccupation with the laparotomy wounds and the epidural often causes us to forget that patients will attach meaning to any unpleasant sensory information following surgery, even for issues that we would regard as minor compared with the pain they would be experiencing if they had not had the epidural. This is why patient-centered care is much more successful than clinician-centered care in helping people.
That patients would expect to not feel any abnormal sensations after surgery confuses doctors and nurses who work in the healthcare setting on a daily basis, as people who have been trained in the use of analgesics appreciate quite readily that these medications cannot abolish pain completely. I think it sometimes doesn’t occur to healthcare workers that while we have become rooted in a culture that understands a vast amount about how the human body functions, our understanding is sometimes imperfect. When I teach neurosurgeons, for example, I point out that when they look at their hands what they see are structures and nerves that provide sensation to those structures. They understand how tendons located in the forearm make fingers move. It is therefore not surprising to them that if a nerve is damaged at the elbow, the function of the hand is affected. Most laypeople, however, have a more rudimentary understanding of how their body functions, with beliefs that are often fixed in urban legend rather than in science, in the same way that the gasoline engine or the inner workings of a computer are a mystery to me. It is therefore our privilege and responsibility as healthcare professionals to translate medical information into language that paints a lucid picture. I sometimes think that, just as some universities have a professor of the public understanding of philosophy and science, there should exist a faculty for training individuals who aim to bridge the chasm between the science of medicine and its intended beneficiaries. Regrettably, many believe that doctors naturally bridge this chasm.
While patients may not need to understand the details of the circuits and molecules involved in producing the experience of pain, as I have described in this chapter, it is important that they understand how powerfully their interpretation of what they are feeling impacts on their pain. An understanding of the role of thoughts and feelings will enable the person suffering to manage their expectations regarding pain and its treatment. While the distress associated with the pain experience is normal and often useful, as it can provide crucial information and lead an individual to seek appropriate help, a good understanding of what influences pain and why can be hugely beneficial in both managing pain and even decreasing it (by reducing feelings of being overwhelmed and distressed). Pain is, after all, both a sensory and an emotional experience, with the initial information regarding the damage activating various parts of the brain and triggering a complex physiological and psychological response. It is only by addressing the complete experience of pain that we can hope to manage pain and alleviate suffering.
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