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The hazards of congenital insensitivity to pain (CIP) are well-known.
This question is about the obverse: what selective advantage, if any, does the normal sensation of pain confer? I'm thinking of severe pain such as that associated with back injury, burns, and some intestinal problems in which the pain seems to serve no function other than to incapacitate.
A related question is whether there is a spectrum of sensitivity to pain, ranging from CIP to heightened sensitivity, what the distribution looks like, and whether this is a genetically plastic trait (like color perception)? If the distribution were sensitive to selective pressure then naively I would guess it serves our needs well, but we spend a lot of our collective time trying to dial it back, hence my question.
Yes a range of pain exists. This can be seen probably in your friends who all probably have a completely different threshold for pain. When doctors ask patients to rate their pain it's usually to establish a baseline so after treatment we can see if there's a decrease. The different thresholds have so many factors from general health to receptors to brain activity to emotional state. You name it! Often just focussing on a pain makes it more painful.
It's definitely an unpleasant sensation pain but it's our way of our body saying "hey, you need to pay attention". Usually the response required is rest or to identify what might be there causing the pain. For example pain means we will withdraw very quickly from a hot surface. Doesn't even require the brain as it is a reflex arc which minimises the time we spend burning that part of our body. And as it continues to hurt we use the arm less letting it recover and protecting it from infection by doing so. As these hazards of being cut, burnt, bit, knocked, fractured are very common there is a survival advantage to be the individual that is alerted to these hazards and take the necessary actions. Particularly in children where pain is necessary as it makes the baby know it needs to eat (or the mother) or that something isn't a good idea (putting hands on something hot).
However as you say there are times when the pain itself is more crippling than anything else and in that situation we have a problem. Childbirth, backache and in cancer or in tension headaches are just some examples. As being able to feel pain is pretty much required for a long life, the disadvantage of having pains like the above is less and doesn't outweigh the benefits. Pain is always going to be necessary. They also usually don't interfere with reproduction and so genes are passed on.
In terms of inflammation, the purpose of pain is to force the organism to rest the area that is inflamed. Thus promoting healing. In terms of chronic pain, this is the same thing. However I think that if the pain will not cease regardless of protection of the affected area, and say if the underlying cause of the pain is ultimately fatal, then the pain is subordinate. The phenotype is already being selected out.
I think the concept shows a lot of parallel to the underlying concept of hypersensitivity (allergy).
Remember that over generations as all different things that can cause and prevent pain in our bodies are evolving, So too is the pain mechanism itself evolving.
The Health Benefits of Corydalis
Emily Dashiell, ND, is a licensed naturopathic doctor who has worked in group and private practice settings over the last 15 years. She is in private practice in Santa Monica, California.
Verywell / Anastasia Tretiak
Corydalis (Corydalis yanhusuo) is a species of flowering herbal plants in the Papaveraceae family, which belong to the Ranunculales order (often called poppies). Corydalis can be found in the Northern Hemisphere, but they are most prevalent in high-altitude grasslands in China's province of Zhejiang.
The flower itself typically consists of five to 15 purple-blue-hued flowers clustered together that curve outward. Corydalis should not be confused with Corydalus, which is a genus of large flying insects known as dobsonflies found in North, Central, and South America.
Mutations in the NTRK1 gene cause CIPA. The NTRK1 gene provides instructions for making a receptor protein that attaches (binds) to another protein called NGFβ. The NTRK1 receptor is important for the survival of nerve cells (neurons ).
The NTRK1 receptor is found on the surface of cells, particularly neurons that transmit pain, temperature, and touch sensations (sensory neurons). When the NGFβ protein binds to the NTRK1 receptor, signals are transmitted inside the cell that tell the cell to grow and divide, and that help it survive. Mutations in the NTRK1 gene lead to a protein that cannot transmit signals. Without the proper signaling, neurons die by a process of self-destruction called apoptosis. Loss of sensory neurons leads to the inability to feel pain in people with CIPA. In addition, people with CIPA lose the nerves leading to their sweat glands , which causes the anhidrosis seen in affected individuals.
Learn more about the gene associated with Congenital insensitivity to pain with anhidrosis
Pain Is Necessary for Survival, but Our Brain Can Stop It if It Needs To
In April 2003, the climber Aron Ralston found himself at the floor of Blue John Canyon in Utah, forced to make an appalling choice: face a slow but certain death—or amputate his right arm. Five days earlier he fell down the canyon—since then he had been stuck with his right arm trapped between an 800-lb boulder and the steep sandstone wall. Weak from lack of food and water and close to giving up, it occurred to him like an epiphany that if he broke the two bones in his forearm he could manage to cut off the rest with his pocket knife. The thought of freeing himself and surviving made him so exited he spent the next 40 minutes completely engrossed in the task: first snapping his bones using his body as a lever, then sticking his fingers into the arm, pinching bundles of muscle fibers and severing them one by one, before cutting the blue arteries and the pale “noodle-like” nerves. The pain was unimportant. Only cutting through the thick white main nerve made him stop for a minute—the flood of pain, he describes, was like thrusting his entire arm “into a cauldron of magma.” Finally free, he rappelled down a cliff and walked another 7 miles until he was rescued by some hikers (Ralston, 2010).
How is it possible to do something so excruciatingly painful to yourself, as Aron Ralston did, and still manage to walk, talk, and think rationally afterwards? The answer lies within the brain, where signals from the body are interpreted. When we perceive somatosensory and nociceptive signals from the body, the experience is highly subjective and malleable by motivation, attention, emotion, and context.
Figure 3. Pain processing pathways. Left – Ascending pain pathways: An injury is signaled simultaneously via fast-conducting Aα or Aβ-fibres and slow-conducting C-pain or Aδ-fibres. The fast A-fibres signal pressure, stretching and other tissue movements to the somatosensory cortex via the dorsal column nuclei. The C-pain and Aδ-fibres sends pain information from nociceptors in the tissue or skin, and transmits these signals to second order neurons in the dorsal horn of the spinal cord. The second order neurons then cross over to the opposite side, where they form the ascending spinothalamic tract. This tract projects signals to nuclei in the medulla and midbrain on the way up to the thalamus (T). The thalamus relays the information to the somatosensory and insular cortex, as well as cortical regions mediating different aspects of the pain experience such as affective responses in the cingulate cortex. Right – Descending pain modulation pathways: Information from the environment and certain motivational states can activate this top–down pathway. Several areas in the limbic forebrain including the anterior cingulate and insular cortex, nuclei in the amygdala and the hypothalamus (H), project to the midbrain periaqueductal grey (PAG), which then modulates ascending pain transmission from the afferent pain system indirectly through the rostral ventromedial medulla (RVM) in the brainstem. This modulating system produces analgesia by the release of endogenous opioids, and uses ON- and OFF-cells to exert either inhibitory (green) or facilitatory (red) control of nociceptive signals at the spinal dorsal horn.
Somatosensation includes all sensation received from the skin and mucous membranes, as well as from the limbs and joints. Somatosensation occurs all over the exterior of the body and at some interior locations as well, and a variety of receptor types, embedded in the skin and mucous membranes, play a role.
There are several types of specialized sensory receptors. Rapidly adapting free nerve endings detect nociception, hot and cold, and light touch. Slowly adapting, encapsulated Merkel’s disks are found in fingertips and lips, and respond to light touch. Meissner’s corpuscles, found in glabrous skin, are rapidly adapting, encapsulated receptors that detect touch, low-frequency vibration, and flutter. Ruffini endings are slowly adapting, encapsulated receptors that detect skin stretch, joint activity, and warmth. Hair receptors are rapidly adapting nerve endings wrapped around the base of hair follicles that detect hair movement and skin deflection. Finally, Pacinian corpuscles are encapsulated, rapidly adapting receptors that detect transient pressure and high-frequency vibration.
PATHWAYS OF PAIN
Pain patlevvays were seen as leaving three components:-
A first order neurone (cell body in dorsal root ganglion) which transmits pain from a peripheral receptor to a second-order neurone.
A second-order neurone in the dorsal horn of the spinal cord, uheicle axon crosses the midline to ascend in the spinothalamic tract to the thalamus where a third neurone.
A third-order neurone projects to the postcentral gyros (via the internal capsule).
There is some evidence that neurotransmitters such as substance P (=sP), vasoactive intestinal polypeptide (VIP) and calcitonin gene-related peptide are important mediators, either as neurotransmitters, or sensitisers of visceral pain receptors.
Prostaglandins, histamine, serotonin, bradykinin, ATP, potassium, and H+ ions also appear important in this regard, especially serotonin, which appears to act mainly on 5HT3 receptors.
In terms of pain perception, thresholds for feeling pain are remarkably constant from individual to individual. i.e. Peripheral receptor stimulation of sufficient intensity will reproducibly cause pain at the same level in most people.
The response of the individual, and his tolerance of the pain, will however differ markedly between individuals. Of great interest is “Neurogenic Inflammation”. Here, stimulation of C fibres causes a local reaction consisting of vasodilatation and increased capillary permeability.
This is due to retrograde transport and local release of sP and calcitonin gene-related peptide. As a consequence, K+, H+, acetylcholine, histamine and bradykinin may be released, and these in turn cause prostaglandin and leukotriene production (which may end up sensitizing high-threshold mechanoreceptors.
Analgesic drugs that act peripherally include non-steroidal anti-inflammatory agents, corticosteroids, local anaesthetic agents (which may theoretically inhibit neurogenic inflammation if given early enough, an area of great controversy), and even novel drugs such as substance P antagonists.
Advantages of pain sensation? - Biology
Central sensitization is a condition of the nervous system that is associated with the development and maintenance of chronic pain. When central sensitization occurs, the nervous system goes through a process called wind-up and gets regulated in a persistent state of high reactivity. This persistent, or regulated, state of reactivity lowers the threshold for what causes pain and subsequently comes to maintain pain even after the initial injury might have healed.
Central sensitization has two main characteristics. Both involve a heightened sensitivity to pain and the sensation of touch. They are called allodynia and hyperalgesia. Allodynia occurs when a person experiences pain with things that are normally not painful. For example, chronic pain patients often experience pain even with things as simple as touch or massage. In such cases, nerves in the area that was touched sends signals through the nervous system to the brain. Because the nervous system is in a persistent state of heightened reactivity, the brain doesn't produce a mild sensation of touch as it should, given that the stimulus that initiated it was a simple touch or massage. Rather, the brain produces a sensation of pain and discomfort. Hyperalgesia occurs when a stimulus that is typically painful is perceived as more painful than it should. An example might be when a simple bump, which ordinarily might be mildly painful, sends the chronic pain patient through the roof with pain. Again, when the nervous system is in a persistent state of high reactivity, it produces pain that is amplified.
Chronic pain patients can sometimes think they must be going crazy because they know intellectually that touch or simple bumps shouldn’t be as uncomfortable or painful as they experience them. Other times, it’s not the patients themselves who think they are crazy, but their friends and loved ones. Friends and loved ones can witness the chronic pain patient grimacing at the slightest touch or crying out at the simplest bump and they think that the chronic pain patient must really be a hypochondriac or something. After all, the contrast between them and the chronic pain patient is stark: the friends and loved ones can be touched or get a bump and it doesn’t send them through the roof. The difference, though, is that the friends and loved ones don’t have a nervous system that is stuck in a persistent state of heightened reactivity, called central sensitization.
In addition to allodynia and hyperalgesia, central sensitization has some other characteristics, though they may occur less commonly. Central sensitization can lead to heightened sensitivities across all senses, not just the sense of touch. Chronic pain patients can sometimes report sensitivities to light, sounds and odors. 1 As such, normal levels of light can seem too bright or the perfume aisle in the department store can produce a headache. Central sensitization is also associated with cognitive deficits, such as poor concentration and poor short-term memory. 2 Central sensitization also corresponds with increased levels of emotional distress, particularly anxiety. 3 After all, the nervous system is responsible for not only sensations, like pain, but also emotions. When the nervous system is stuck in a persistent state of reactivity, patients are going to be literally nervous – in other words, anxious. Lastly, central sensitization is also associated with sick role behaviors, such as resting and malaise, 4 and pain behavior. 5, 6
Central sensitization has long been recognized as a possible consequence of stroke and spinal cord injury. However, it has become increasingly clear that it plays a role in many different chronic pain disorders. It can occur with chronic low back pain, 7, 8 chronic neck pain, 9 whiplash injuries, 10 chronic tension headaches, 11, 12 migraine headaches, 13 rheumatoid arthritis, 14 osteoarthritis of the knee, 15 endometriosis, 16 injuries sustained in a motor vehicle accident, 17 and after surgeries. 18 Fibromyalgia, 19 irritable bowel syndrome, 20 and chronic fatigue syndrome, 21 all seem to have the common denominator of central sensitization as well.
What causes central sensitization?
Central sensitization involves specific changes to the nervous system. Changes in the dorsal horn of the spinal cord and in the brain occur, particularly at the cellular level, such as at receptor sites. 3, 22
As stated above, it has long been known that strokes and spinal cord injuries can cause central sensitization. It stands to reason. Strokes and spinal cord injuries cause damage to the central nervous system – the brain, in the case of strokes, and spinal cord, in the case of spinal cord injuries. These injuries alter the parts of the nervous system that are directly involved in central sensitization.
But what about the other, more common, types of chronic pain disorders, listed above, like headaches, chronic back pain, or limb pain? The injuries or conditions that lead to these types of chronic pain are not direct injuries to the brain or spinal cord. Rather, they involve injuries or conditions to the peripheral nervous system – that part of the nervous system that lies outside the spinal cord and brain. How do injuries and conditions associated with the peripheral nervous system lead to changes in the central nervous system, which, in turn, lead to chronic pain in the isolated area of the original injury? In short, how do isolated migraine headaches become chronic daily headaches? How does an acute low back lifting injury become chronic low back pain? How does an injury to a hand or foot become a complex regional pain syndrome?
There are likely multiple factors that lead to the development of central sensitization in these so-called ‘peripheral’ chronic pain disorders. These factors might be divided into two categories:
- Factors that are associated with the state of the central nervous system prior to onset of the original injury or pain condition
- Factors that are associated with the central nervous system following onset of the original injury or pain condition
The first group involves those factors that might predispose patients to developing central sensitization once an injury occurs and the second group involves antecedent factors that foster central sensitization once pain starts.
There are likely both biological, psychological, and environmental predisposing factors.
Low and high sensitivity to pain, or pain thresholds, are likely in part due to multiple genetic factors. 1 While there is no research as of yet to support a causal link between pre-existing pain thresholds and subsequent development of central sensitization following an injury, it is largely assumed that one will be found.
Psychophysiological factors, such as the stress-response, are also apt to play a role in the development of central sensitization. Direct experimental evidence on animals 23, 24 and humans, 25, 26 as well as prospective studies on humans, 27 have shown a relationship between stress and lowering of pain thresholds. Similarly, different types of pre-existing anxiety about pain is consistently related to higher pain sensitivities. 28, 29 All these psychophysiological factors suggest that the pre-existing state of the nervous system is an important determinant of developing central sensitization following the onset of pain. It stands to reason. If the stress response has made the nervous system reactive prior to injury, then the nervous system might be more prone to become centrally sensitized once onset of pain occurs.
There is considerable indirect evidence for this hypothesis as well. A prior history of anxiety, physical and psychological trauma, and depression are significantly predictive of onset of chronic pain later in life. 30, 31, 32, 33 The common denominator between chronic pain, anxiety, trauma, and depression is the nervous system. They are all conditions of the nervous system, particularly a persistently altered, or dysregulated, nervous system.
It's not that such pre-existing problems make people more prone to injury or the onset of illness -- as injury or illness is apt to occur on a somewhat random basis across the population. Rather, these pre-existing problems are apt to make people prone to the development of chronic pain once an injury or illness occurs. The already dysregulated nervous system, at the time of injury, for instance, may interfere with the normal trajectory of healing and thereby prevent pain from subsiding once tissue damage heals.
Factors leading to central sensitization following onset of pain
Antecedent factors can also play a role in the development of central sensitization. The onset of pain is often associated with subsequent development of conditions such as depression, fear-avoidance, anxiety and other stressors. The stress of these responses can, in turn, further exacerbate the reactivity of the nervous system, leading to central sensitization. 3, 34
Poor sleep is also a common consequence of living with chronic pain. It is associated with increased sensitivity to pain as well. 35, 36
In what’s technically called operant learning, interpersonal and environmental reinforcements have long been known to lead to pain behaviors, but it is also clear that such reinforcements can lead to the development of central sensitization. 37, 38, 39
Treatments of central sensitization
Treatments for chronic pain syndromes that involve central sensitization typically target the central nervous system or the inflammation that corresponds with central sensitization. These are antidepressants, 40 and anticonvulsant medications, 41, 42, 43 and cognitive behavioral therapy. 44, 45, 46 While usually not considered to target the central nervous system, regular mild aerobic exercise alters structures in the central nervous system 47, 48 and leads to reductions in the pain of many conditions that are mediated by central sensitization. As such, mild aerobic exercise is used to treat chronic pain syndromes marked by central sensitization. 49 Non-steroidal anti-inflammatories are used for the inflammation associated with central sensitization. 3
Lastly, chronic pain rehabilitation programs are a traditional, interdisciplinary treatment that uses all of the above-noted treatment strategies in a coordinated fashion. They also take advantage of the research on the role of operant learning in central sensitization and have developed behavioral interventions to reduce the associated pain and suffering. 50, 51 Such programs are typically considered the most effective treatment option for chronic pain syndromes. 52, 53, 54, 55
For more information, please see these related topics: the neuromatrix of pain, the changing paradigms in chronic pain management, and the mission of the Institute for Chronic Pain to educate the public about empirical-based conceptualizations of pain and its treatments.
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Why therapists need a philosophy of pain
A very special guest post from three very high calibre thinkers, philosophers and clinicians. My sincere thanks to Julian Kiverstein, Laura Rathbone and Mick Thacker for sharing their post with us, so that we can have the pleasure of sharing it with you.
Traditionally physiotherapists (and other physical or manual therapists) have focused on treating tissue damage, not the person with pain. However, to treat the person, and not only the part of them that hurts, clinicians need to make sense of the highly complex experience of being in pain.
Many patients with chronic pain experience pain from the moment they wake until the moment they fall asleep. Pain penetrates every experience they have of the world. Their ability to work, take care of their children, exercise and enjoy the company of friends can suddenly be lost to them. In short, little of their lives is untouched by their experience of being in pain. They may struggle to retain a grip on the life they led before pain took hold of them. Faced with such a complex experience, patients may look to clinicians to make sense of this for them.
Clinicians may try to answer their patient’s questions about pain by reaching for an objective, scientific and biomedical model of pain. They may have been trained for instance to think of pain as like an alarm system warning of tissue damage. Clinicians use this model to explain to patients what they are experiencing and how they will treat them. The trouble is the model therapists have been taught inevitably leaves much unexplained, both for the clinician and the patient.
According to the popular biomedical model, pain hurts when your brain reaches the conclusion that bodily tissue needs protecting from an external threat. Central to the biomedical model of pain are so-called nociceptors: nerves cells dedicated to the detection of potential or actual damage to or inflammation of bodily tissue. The nociceptive system is just one of the many systems that evolution has equipped us with to protect our bodies. The body’s immune system, motor system and sympathetic nervous system also have this function. Pain experience is somehow the product of these multiple systems working together.
According to the popular biomedical model, pain hurts when your brain reaches the conclusion that bodily tissue needs protecting from an external threat.
The “somehow” is the crucial word in this statement of the biomedical model: how does the activity of these multiple systems explain the single, complex pain experience the subject undergoes? Far from helping the patient to make sense of their pain, the biomedical model threatens to engender only more confusion.
Many therapists have long ago given up on the biomedical model opting for a substantial nuancing and hedging of the core tenets of this model. They suggest instead that pain is a complex experience built out of biological, cognitive psychological, and social components. However, each of these components disguises yet more complexity. Both patient and clinician immediately run into the same puzzle that hampers the biomedical model. The problem is to understand how all of these parts are combined to produce the patient’s complex experience.
Consider first what is known about the biology of pain. The biological elements include the brain’s sensory-discriminative systems that process somatosensory signals from the body. These signals carry information about mechanical disturbances, temperature increases, and concentration of chemical irritants impinging on the body. The neurons that make up this system can become increasingly sensitised and hypervigilant following bodily trauma. The threshold for the triggering of this system may become lowered after injury to the body. This increased sensitivity can have the consequence that the alarm signaling a threat to the body can be sounded when there is no actual threat.
Sensory-discriminative systems are sometimes further distinguished from affective-motivational systems in the brain. The affective dimension of this system is what makes pain unpleasant, a sensation we dislike when it occurs. The motivational component is what moves the person to take action when a potential or actual threat to the body is detected. When in pain the person feels compelled to act in ways that allow them to escape the danger. Pain demands attention, imposing a priority on action systems to take measures to avoid harm.
how does the activity of these multiple systems explain the single, complex pain experience the subject undergoes?
A unified pain experience
Having distinguished these biological components, the question arises again of how they come back together to produce a single unified pain experience. The painfulness (the sensory-discriminative system) and the hurtfulness (the affective-motivational system) of pain are not distinguishable elements in a typical experience. Sensations of pain strongly affect us negatively and at one and the same time they move us to take action. What a person is ready to do and how they are negatively affected is not distinct from the painful subjective sensation the person undergoes. They somehow form a single package.
Nor can the response of these systems be readily disentangled from emotional and cognitive systems – the person’s thoughts, beliefs, hope and fears (so-called cognitive-evaluative aspects of pain). Part of pain experience is what one believes and expects to happen when one interacts with the world. Part of being in pain is to do with the future one imagines for oneself. It could be a future in which they wake up with pain everyday like in our opening example. Such a person might understandably lose hope. Moreover, pain often occurs in the absence of any detectable damage to bodily tissues. The person may be told they are making it up, imagining it, seeking the benefits of illness or disability without entitlement but of course the person is not making it up. If the person believes they are in pain then they are in pain.
No sharp lines
There is no sharp line between pain sensation, and one’s thoughts, beliefs and expectations. Consider in this light placebo and nocebo analgesic responses. Patients in severe pain can report significant pain relief after being given a compound they believe to be a painkiller. The opposite effect can also occur in nocebo analgesic responses in which expectation of harm or threat can result in increased perceived intensity of pain. In the Second World War it has been reported that wounded soldiers in combat hospitals did not require as much analgesia compared to civilians with comparable injuries. The meaning the soldiers gave to their injuries seemed to play a part in how much pain they experienced. For the soldiers injury meant time away from the battlefield and their possible survival. For civilians the same injury had a very different meaning.
Pain experience also has a social dimension. How much pain children report will depend in part in how their parents have reacted in the past to their pain. The amount of social support a person receives can also influence the intensity with which they feel pain. The presence of a loved one can reduce the intensity of a pain experience. Pain can also deprive a person of their place in society. They may find they are unable to go to work or that they avoid meeting with friends out of fear of experiencing pain. They can no longer take part in shared recreational activities such as sport. Pain is isolating insofar as it leads one to withdraw from social life. It may also be the source of embarrassment.
Finally, there is the phenomenological dimension of pain – the first and second-person experience the person has of their surroundings and of other people when they are in pain. The person in pain is both a biological being and a person that experiences a meaningful world through their embodiment in it. The person can adopt these two very different perspectives on their pain. They can experience the pain as part of their lived reality or they can relate to the pain as a disturbance of their physical body.
Still a therapist might wonder: What is the value of a philosophy of pain for clinical practice? Our answer to this question is that how you treat a patient’s pain is always implicitly, if not explicitly, informed by a model or understanding of what pain is.
The problem of parts
How can we adopt these two very different perspectives on one and the same phenomenon, the pain experience? This is of course a version of the famous philosophical mind-body problem: the problem of making sense of how a physical body can also be a subject of experiences, the thinker of thoughts, the feeler of feelings and the agent of actions.
We can see then that both the biomedical and the new improved biopsychosocial models of pain lead to many more questions than they are able to answer. In his book Gut Reactions Jesse Prinz made a distinction between two problems that arise when thinking about emotion. Pain is also a gut reaction, hence these same two problems arise for pain.
The first problem Prinz called the problem of parts. Applied to pain the problem is one of saying which of the components reviewed above is really an essential part of pain and which are effects or modulators of pain. If one adheres to the biomedical model of pain for instance, one might attempt to reduce pain to the biological components we described above. The cognitive psychological, social and phenomenological components would then be treated as modulators of these biological processes. Such a reductive picture of pain leads to a problematic separation of biology from the psychological, social and phenomenological. Therapists need a philosophy of pain that avoids making such separations.
The problem of plenty
The second problem Prinz called the problem of plenty. We have just suggested all of the dimensions of pain described in the biopsychosocial model are essential parts of pain experience. In addition, we would add the phenomenological and existential dimension of being a lived body. The problem of plenty arises when we try to understand how these different parts all hang together to make up a single complex experience of pain. It is by no means a straightforward task to understand how these diverse elements of biological, psychological, social, existential and phenomenological all coalesce to make up a pain experience. Moreover, knowledge of each of these elements is arrived at through very different instruments and practices. The question of how to bring these different ways of knowing together into a single understanding of pain is also no easy task. Both tasks call for a philosophy of pain.
What is the value of a philosophy of pain?
Still a therapist might wonder: What is the value of a philosophy of pain for clinical practice? Our answer to this question is that how you treat a patient’s pain is always implicitly, if not explicitly, informed by a model or understanding of what pain is.
We have already encountered an extreme example above of patients with chronic pain. Suppose you are operating with a model of pain as necessarily tied to the process of detecting tissue damage. The absence of such tissue damage might lead one to think of chronic pain as psychologically motivated in some way. The person presenting with chronic pain may be treated with suspicion, suspected of fabricating, or at the very least of exaggerating the true extent of their pain.
Now consider a philosophy of pain that provides an answer to the problem of plenty by integrating the different dimensions of pain identified above. Such a framework could be valuable for providing multiple perspectives from which to think about the patient’s problem. These different perspectives would allow one a richer set of tools both for making sense of the patient but also for evaluating the effectiveness of one’s treatment. A philosophy of pain can help therapists to understand how the different biological, psychological, social and existential factors influence each other in ways that may contribute to sustaining the experience of pain long after the physiological damage to the body has healed.
Last but not least if one has a philosophy of pain that includes the phenomenological and existential dimensions of pain this opens up the possibility of the clinician helping the patient to find ways to live meaningfully despite waking up with pain every morning. Pain introduces a relation of distance between the person and their body in the sense that the body is no longer something the person can simply take for granted in their dealings with the world. The body no longer “passes us by in silence” to borrow Sartre’s words. The body becomes the focus of the person’s concern.
A philosophy of pain can therefore allow for a different therapeutic relationship with their patients. Therapists can help patients to cultivate skills and capacities for living full and rich lives that creatively adapts to their pain
Finding possibilities for living a full life
A philosophy of pain allows both patient and clinician to take different perspectives on the body. The clinician can help the patient to view their pain as a part of their physical body but not necessarily as defining their lived reality. A person can find possibilities for living a full life even while they are still suffering with pain. One might think that being in pain excludes living well but this is not necessarily the case. Pain need not be viewed as the mutually exclusive opposite of being well and living a meaningful life. A philosophy of pain can therefore allow for a different therapeutic relationship with their patients. Therapists can help patients to cultivate skills and capacities for living full and rich lives that creatively adapts to their pain.
Julian Kiverstein, Laura Rathbone and Mick Thacker (2021)
Julian Kiverstein is Senior Researcher at the department of psychiatry, Amsterdam University Medical Centre. He is trained as a philosopher but works now at the intersection between philosophy, theoretical neurobiology, psychiatry and embodied cognitive science. He has published widely including a monograph titled Extended Consciousness and Predictive Processing: a Third Wave View (co-authored with Michael Kirchhoff).
Laura Rathbone is a Physiotherapist and Coach working with people experiencing complex and persisting pain alongside other symptoms. She guest lectures on physiotherapy, pain and whole-person care. She hosts the podcast Philosophers Chatting with Clinicians, curates the community reading group Pain Geeks and is part of the Le Pub Scientifique team.
Mick Thacker is Professor of Physiotherapy, Pain and Rehabilitation at London South Bank University. Mick has performed Doctoral level studies within the fields of neuro-immunology and philosophy of pain, and Post-Doctoral research in neuroimaging. He is a keen explorer of, and advocate for a new and better understanding of pain and the need to develop new pain management strategies. This has led Mick to develop a particular interest in Predictive Processing (PP) and its application in facilitating a better understanding of pain affecting individuals and wider society.
My very special thanks again to Julian, Laura and Mick for sharing this post with us on noijam. As good philosophical thinking and writing should, the piece will challenge and confront, at the same time as requiring you to question, think and reflect. Civil, constructive comments and discussion are welcome below.
If you want more Julian, Laura and Mick, you can listen to a fantastic conversation between the three of them on Laura’s Philosophers Chatting with Clinicians podcast.
If you would like to dive deeper into Predictive Processing and pain, Mick and Julian, together with Michael Kirchhoff have just published a landmark paper Why Pain Experience is not a Controlled Hallucination of the Body, available open access here.
Mutations in the SCN9A gene cause congenital insensitivity to pain. The SCN9A gene provides instructions for making one part (the alpha subunit) of a sodium channel called NaV1.7. Sodium channels transport positively charged sodium atoms (sodium ions) into cells and play a key role in a cell's ability to generate and transmit electrical signals. NaV1.7 sodium channels are found in nerve cells called nociceptors that transmit pain signals to the spinal cord and brain. The NaV1.7 channel is also found in olfactory sensory neurons , which are nerve cells in the nasal cavity that transmit smell-related signals to the brain.
The SCN9A gene mutations that cause congenital insensitivity to pain result in the production of nonfunctional alpha subunits that cannot be incorporated into NaV1.7 channels. As a result, the channels cannot be formed. The absence of NaV1.7 channels impairs the transmission of pain signals from the site of injury to the brain, causing those affected to be insensitive to pain. Loss of this channel in olfactory sensory neurons likely impairs the transmission of smell-related signals to the brain, leading to anosmia.
Learn more about the gene associated with Congenital insensitivity to pain
Molecular and Cell Biology of Pain
4.4 Other chronic pain states
Neuropathic pain and persistent inflammatory pain are typically modeled in rodents using peripheral nerve trauma via surgical techniques and Complete Freund's Adjuvant (CFA) injection into the hind paw, respectively. Using the spared nerve injury (SNI) and CFA mice models, the numbers of mitochondria in the dorsal horn were visualized following intrathecal administration of a fluorescent mitochondrial marker. 88 Seven days following CFA and 14 days following SNI, there were significant increases in the number of mitochondria in laminae I–V of the ipsilateral side of the spinal cord compared to the contralateral side. 88 Up to day 7 following partial sciatic nerve ligation (PSNL), an increase in cytochrome c levels in the spinal cord was reported 89 indicating mitochondrial dysfunction as cytochrome c is normally contained within the inner and outer mitochondrial membranes. Furthermore, systemic administration of cyclosporin A, an mPTP blocker, pre- and post-PSNL inhibited PSNL-evoked mechanical allodynia. 89
The majority of the studies that suggest a potential role of mitochondrial dysfunction in neuropathic and inflammatory pain have focussed on ROS and oxidative stress. CCI-evoked heat hyperalgesia could be inhibited by antioxidants TEMPOL, 90 N-acetylcysteine, 91 and tirilazad. 92 In addition, increased SOD-2 levels were found in the axotomized sciatic nerve. 93 PBN, a nonspecific ROS scavenger, inhibited mechanical hypersensitivity evoked by spinal nerve ligation, 94–96 capsaicin-induced inflammation, 22,97 and visceral inflammation. 98 Other nonspecific ROS scavengers, 5,5-dimethylpyrroline-N-oxide and nitrosobenzene also relieved neuropathic pain behaviors. 94 Reagents that mimic SOD-2 activity inhibited hypersensitivity to mechanical/heat stimuli evoked by either peripheral nerve injury 90,96 or inflammation. 22,97,99,100 Finally, mitochondrial ROS-producing profiles, visualized through in vivo delivery of a fluorescent mitochondrial marker, were increased in the spinal cord following peripheral nerve injury 101 or an inflammatory stimulus. 22,23