A thought-provoking book that should be read by anyone interested in the study and management of pain.
I provide select passages from the book and will update with additional quotes in the future.
Note: the book passages included or highlighted in this article do not indicate I endorse the wording or viewpoints; they are included for the benefit of potential readers of the book.
It is useful to read books and articles that provide an interesting and, at times, critical perspective on your area of research. To this end, I recently read The Right to Pain Relief and Other Deep Roots of the Opioid Epidemic by Mark Sullivan and Jane Ballantyne.
- The Right to Pain Relief and Other Deep Roots of the Opioid Epidemic
- Authors: Mark Sullivan and Jane Ballantyne
- https://academic.oup.com/book/45507
Below are select quotes from the book (italics mine) that introduce or discuss to concepts that might clash with how others might view pain as a percept along with the evolutionary or functional reasons for persistent (or chronic) pain after an injury has apparently healed. Other quotes are just of general interest. The book also includes two epilogue chapters with perspectives on pain from a clinician and patient; it would have been nice to have additional perspectives covering an even wider range of conditions, treatments, and views.
The book is worth reading for those who study and treat pain. It is likely a good starting point for more in-depth discussions, e.g. if select passages are chosen for review and comments in journal club-style meetings or other settings.
Book quotes
Multidisciplinary pain rehabilitation programs and cognitive–behavioral treatments (CBT) of chronic pain often produce earlier and more marked reductions in pain-related disability than pain intensity.27,28 The 2020 Cochrane review of CBT trials reports that CBT reduces pain and distress and disability by only small or very small amounts.29 Thus, many of our best chronic pain treatments do not affect pain intensity ratings substantially or primarily. This suggests that pain intensity reduction may not be the primary or sole goal for chronic pain treatment.
A critique of chronic pain as disease Despite its broad support within the professional pain community, there are multiple reasons to question the assertion that chronic pain is a disease. Cohen and colleagues articulated one of these succinctly in their question, “To what extent does the theory of pain-as-a-disease offer an explanation of pain?”48 The pain-as-disease proponents cited above point to abnormalities on structural and functional neuroimaging as well as corroborating neurophysiology and neurochemistry studies to argue that there is identifiable neuropathology that causes chronic pain. The presence of this neuropathology has been found by multiple investigators using multiple methods, so it can be considered a valid finding. The problem is that pain is asserted to be both the cause and the effect of this neuropathology. As Cohen and colleagues state, “By asserting that pain is an agent that can cause a disease also called ‘pain,’ the proponents of this theory have fallen foul of circular argument.” [...] It is not clear what the pain-causing and/or pain-caused neuropathology adds to the explanation of chronic pain.
Moseley and Butler is opposed to the idea that acute pain is nociceptive, while much of chronic pain is not. Because he conceives of the pain system as protecting against danger, not just damage, he does not distinguish between eudynia (helpful acute pain) and maldynia (unhelpful chronic pain).16 EP sees all clinical pain as cognitively modulated. This modulation is not limited to chronic pain; it affects not just the interpretation of pain, but its intensity.
Pain is primarily imperative rather than informative The focus on pain’s role in our survival represents a fundamental reconception of pain. [...] Pain’s function, on the Cartesian view, is to provide information about the world that is outside our mind. Specifically, it provides information about damage to our body. But what if these standard views of pain’s function are seriously mistaken? [...] Klein argues that the primary function of pain is to command protective behavior rather than to inform us of tissue damage. [...] “Ordinary sensations inform but don’t necessarily motivate. Pains motivate without informing. That is why pain is unusual.”
This delayed protective pain can persist when safety has not been restored. The traditional distinction between acute and chronic pain relies on the idea of tissue healing time. On the traditional view of pain as a sign of tissue damage, when the tissue damage has healed, pain should cease. According to Bonica, chronic pain is pain that persists beyond healing time.30 But the imperative, danger-focused pain theory offers an alternative understanding. Pain persists when danger to integrity persists. This can occur due to properties of the body (e.g., persistent inflammation), the person (e.g., history of psychological trauma), or the situation (e.g., ongoing threat of domestic violence). [...] pain is more about action than information. Pain commands protective action. It is informative (e.g., about location or type of injuring agent) only insofar as that is necessary for effective protective action. Pain not only prompts protective movement [...], but it also can itself be understood as a form of protective action. Pain is not imposed on the body; rather, it is something the body does to protect itself. Injury may happen to an animal, but pain is something the animal produces to survive.
Our mammalian pain system is more clever than the hard-wired labeled lines proposed by specificity theory. It is even more clever than the pain matrix theory that proposed a network of dedicated somatosensory centers in the brain. Our pain system utilizes a “salience network” that allows nociception to be integrated with information from other sensory modalities. Nociception may or may not lead to pain, depending on whether the pain experience helps promote survival. Pain is thus something done by the organism that flexibly promotes protective action to preserve internal homeostatic integrity.
How much pain control is too much pain control? Pain and suffering are inescapable, even valuable, aspects of human life. Any quest for their elimination will distort life. The goal of a “pain-free life” is not a good one. The utilitarians were mistaken about this.
We are certainly not advocating that clinicians start with doubt about patients’ pain complaints. In established outpatient practice, malingering is very rare. We are strongly arguing against the idea that patients’ pain can or should be validated through correspondence with tissue damage. Assessing the “reality” of the patient’s pain is not the central challenge of chronic pain care. Validating pain through functional MRI scans of patients’ brains is as big a mistake as validating back pain through structural MRI scans of patients’ spines.
Clifford Woolf, the physician who discovered and defined the physiology of central sensitization, has said as much in a recent review: “If activity in the forebrain circuits that drive mood and anxiety can alter nociceptive neuronal responsiveness, then this is, I consider, another cause of central sensitization, this time with a central rather than a peripheral driver.”
As Casey states, we investigate pain in order to control it, seeking to identify unique molecular mechanisms, receptors, pathways, and brain centers for pain so we can target these with therapies.
We think of pain and pleasure as feelings, long considered opposites. Yet the feelings of pain and pleasure cannot be understood in isolation from the organism’s and the species’ quest for survival. Pain is not just a feeling, but also a behavioral drive.24 As Porreca and Navratilova have recently written, “Pain is a call to action. Like hunger, thirst, and desire for sleep, pain is a part of the body’s survival systems that collectively are responsible for protecting the organism.”25(pS45) This emotional-drive aspect of pain has been recognized since 1968 when Melzack and Casey replaced a purely sensory model of pain with a multidimensional model that recognized not only sensory/discriminative aspect of pain but also affective/motivational features.26
The link between pain and protection helps explain the variable relationship between pain and tissue damage. “Painless injury occurs … precisely when such protective actions would be maladaptive by prohibiting the necessary avoidance of dangerous situations. When safety should take priority over protection, injury may end up painless.”27(p32) A classic example of painless injury occurs when an animal is injured while fleeing a predator. The animal’s endogenous opioid system suppresses pain until the animal is safe from the predator and protection of the injured body part again becomes most important for survival.29
Healing from physical trauma is relatively simple, and predictable enough that it is reasonable to assume that healing is complete 3 months after the trauma. This is the concept of “healing time” that Bonica used to distinguish acute from chronic pain. Healing from psychological trauma is not so simple or predictable.
If pain is a homeostatic emotion (concerning threats to bodily and personal integrity) like anxiety and depression, and they all share a common neurobiology, we understand them as a continuum of danger warnings, not as sensation and reaction. These homeostatic emotions have been honed through millions of years of natural selection to more efficiently support survival than any line-labeled system (pain vs. touch; nociceptive transmission vs. pain perception) that rigidly separates the processing of physical pain and social pain. As we have seen, pain can arise from physical or psychological trauma or both. Chronic pain remains a frustrating and intriguing clinical problem because it cannot be simply attributed to peripheral broken body parts or to centralized psychological states; often both are involved. Contrary to Descartes, clinical pain is continuously modulated by both the intrabody homeostatic environment and the interpersonal social environment. The endogenous opioid system is one of the principal means by which this modulation occurs. This is the main reason why opioids are such a potent pain treatment, and why they can be so harmful to full human functioning when used continuously and in the long term.
Clinicians must hold patients accountable for their recovery without blaming them for their illness. This balance is also essential for successful care of addicted patients and includes “an attitude of calm respect, that helps them both think and talk with [patients] about their responsibility for harmful behavior, without blaming them.”58(p1150) Compassion and empathy are effective antidotes to blaming. They are achieved by listening to and understanding the patient’s story, including stories of both physical and psychological trauma and any accompanying protective homeostatic emotions like anxiety and depression. The focus is not upon validating pain by tying it to an adequate physical cause (as per above discussions of pain stigma), but in validating and addressing the sources of danger in the patient’s life: “What is making you feel unsafe as a body and a person these days?”
This combo worked really well to keep my pain level down and let me do what I wanted to do. I was able to work all day at my job and still feel good enough to have fun with Vicki. I took my OxyContin in the morning and evening, and carried some Percocet in my pocket for when I needed pain relief.
Full versions of select quotes
For ease to readers, some of the above quotes were abbreviated (e.g. as indicated by [...]
). I have provided the full quotes below for several of those passages in the book.
Pain is primarily imperative rather than informative The focus on pain’s role in our survival represents a fundamental reconception of pain. Since Descartes, we have considered pain to be a sensory experience that represents the state of our body for our mind. Pain’s function, on the Cartesian view, is to provide information about the world that is outside our mind. Specifically, it provides information about damage to our body. But what if these standard views of pain’s function are seriously mistaken? In What the Body Commands: The Imperative Theory of Pain, philosopher Colin Klein argues that “[a]ll pains have imperative content, and that imperative content is what distinguishes them as pains.”27(p1) An imperative is a command, not a representation or a description. Klein argues that the primary function of pain is to command protective behavior rather than to inform us of tissue damage. This may seem like a trivial or nitpicking distinction, but it is not. Most sensory experiences, such as visual and auditory (olfaction may be an exception28), inform us of the outside world, but pain does not. “Ordinary sensations inform but don’t necessarily motivate. Pains motivate without informing. That is why pain is unusual.”27
This delayed protective pain can persist when safety has not been restored. The traditional distinction between acute and chronic pain relies on the idea of tissue healing time. On the traditional view of pain as a sign of tissue damage, when the tissue damage has healed, pain should cease. According to Bonica, chronic pain is pain that persists beyond healing time.30 But the imperative, danger-focused pain theory offers an alternative understanding. Pain persists when danger to integrity persists. This can occur due to properties of the body (e.g., persistent inflammation), the person (e.g., history of psychological trauma), or the situation (e.g., ongoing threat of domestic violence). As we have seen in the case of Suzanne, danger takes many forms and its perception cannot be understood in purely mechanical terms. The core message for us from Klein’s book is that pain is more about action than information. Pain commands protective action. It is informative (e.g., about location or type of injuring agent) only insofar as that is necessary for effective protective action. Pain not only prompts protective movement (e.g., withdrawing from a flame, avoiding weight bearing on a fractured leg), but it also can itself be understood as a form of protective action. Pain is not imposed on the body; rather, it is something the body does to protect itself. Injury may happen to an animal, but pain is something the animal produces to survive.
We are certainly not advocating that clinicians start with doubt about patients’ pain complaints. In established outpatient practice, malingering is very rare. We are strongly arguing against the idea that patients’ pain can or should be validated through correspondence with tissue damage. Assessing the “reality” of the patient’s pain is not the central challenge of chronic pain care. Validating pain through functional MRI scans of patients’ brains is as big a mistake as validating back pain through structural MRI scans of patients’ spines. Assessing the “reality” of a patient’s depression is similarly not the central challenge of depression care. The central challenge is finding a way for the patient to move his life forward. This may seem nebulous because moving life forward can take many forms: returning to work, having fun, making friends, volunteering, finding new or old hobbies. Increasing the patient’s capacity for personally meaningful action reduces pain salience and often pain intensity.61
So what is the right balance? How much pain control is too much pain control? Pain and suffering are inescapable, even valuable, aspects of human life. Any quest for their elimination will distort life. The goal of a “pain-free life” is not a good one. The utilitarians were mistaken about this. This is because pain and pleasure are not opposites and do not exclude each other; they can increase or decrease together.