Call for Abstracts: Meanings of Pain, Volume III

Sculpture by Fabio Viale

Volume III Topic: Meanings of pain in vulnerable or special patient groups

Series Editor: Dr Simon van Rysewyk
Publisher: Springer

The Meanings of Pain book series describes how the meaning of pain changes pain experience – and people – over time.

Pain in the moment is experienced as immediately distressing or unpleasant. If pain persists over time, more complex meanings about the long-term consequences, or burden of pain, can develop. These meanings can include existential meanings such as despair or loneliness that focus on the person with pain, rather than pain itself.

Meanings of Pain offers a vocabulary of language about pain and meaning. An objective of the series is to stimulate self-reflection on how to use information about meaning in clinical and non-clinical pain settings. The book series is intended for people with pain, family members or caregivers of people with pain, clinicians, researchers, advocates, and policy makers.

Although chronic pain can affect anyone, there are some groups of people for whom particular clinical support and understanding is urgently needed. This applies to “vulnerable” or “special” groups of people and to the question of what pain means to them.

Volume III focuses on describing the meanings of pain in groups of “vulnerable” or “special” people, such as:

  • Infants or children
  • Women
  • Older adults
  • People with a physical or intellectual disability
  • People with a brain injury
  • People diagnosed with a disease
  • Veterans
  • Athletes
  • Workers
  • Addicts
  • People with mental illness or mental disorders
  • Homeless people
  • People in rural or remote communities
  • People in multicultural communities
  • Indigenous peoples

Invited chapter types
The editor Dr Simon van Rysewyk invites contributions for Volume III on the meanings of pain in vulnerable or special patient groups. The following manuscript types will be considered:

  • Original Research (e.g., original clinical, translational, or theoretical research)
  • Reviews (e.g., Systematic Reviews, Meta-analytic reviews, Cochrane type reviews, Pragmatic Reviews)

Authors interested in submitting a chapter for publication in Volume III are invited to submit a 350-word Abstract, which includes the name and contact information of the corresponding author, to:

Dr Simon van Rysewyk

Abstract Deadline: open

“It is my opinion that this … work will stand as the definitive reference work in this field. I believe it will enrich the professional and personal lives of health care providers, researchers and people who have persistent pain and their family members. The combination of framework chapters with chapters devoted to analysing the lived experience of pain conditions gives the requisite breadth and depth to the subject.” – Dr Marc A. Russo, MBBS DA(UK) FANZCA FFPMANZCA, Newcastle, Australia, from the Foreword in Volume II

Humans beings are persons and organisms

Sculpture by Fabio Viale

As organisms, human beings interact with the world and each other through causal mechanisms that control us and every other physical thing. As persons, we act in the world through our thoughts, emotions, attitudes, or desires.

Accordingly, human beings are describable in two distinct, but complementary ways: in terms of the way the world is, through scientific descriptions of the causal mechanisms and laws that explain physical things, or, in terms of the way the world seems, through descriptions of personal experiences and meanings.

One or the other way of describing human beings comes into focus depending on the questions we ask about ourselves or the world. The features of personal experience—thought, feeling, speech and action—are amenable to standard scientific explanation as specific changes in the body. Traditionally, scientific research has had much to say about the physical nature of pain, but much less about the personal experience or meaning of pain. Indeed, the meaning of pain remains a blind spot in knowledge.

A description of a human being as a person means that there is a way of understanding of human beings in which personal experience and meaning, rather than physical causation alone, is needed to answer the question, “What is happening?”

Human persons can distinguish between how things are in the world and how things seem to me. I can recognise within myself a perspective or point of view on the world and identify it as belonging to me. Every person has such a unique perspective; this is partly what it means to be a person rather than a physical thing. In contrast, a scientific description of the world does not presuppose any personal point of view. Physical science does not use words like “I”, “here,” or “now”. Does this mean that “persons” are unobservable to standard quantitative science?

Possibly. Imagine a complete explanation of pain according to the final neurophysiology of pain—whatever it turns out to be. Such an explanation of pain would, to put it very crudely, accurately map specific neurophysiological changes in physical parts in the living human organism and all their true causal interactions across time. However invaluable such an explanation would be to pain medicine, it could not describe the way pain seems to the person who experiences it, for which of the physical objects described in this explanation is me with pain, here, now? Immediate pain always seems a certain way to persons, and this “seeming” determines the experience of the person with pain. In describing personal pain, human beings use language with other meanings than the language used in neurophysiology. The final neurophysiological explanation of pain therefore could explain only one dimension of pain in human beings—the physical dimension—in language that could not capture the personal experience, burden, or meaning of pain.

A philosophical assumption of neurophysiology is that a person is identical with his or her body. Person and body are one and the same thing. In terms of personal experience, however, the identity between person and body escapes personal understanding. For example, when I feel a pain, there is no information or evidence, or nothing that I could discover about my body subsequent to the experience of pain, that could demonstrate it to be false. When I feel a pain, I simply know that I am in pain.

In person to person interactions, we commonly respond to each other as though we are not identical with the human body, but in a compelling sense operating “through” the body, which seems to be a vehicle of thought, emotion, pain or suffering. We feel that each person we encounter in the world is a unique perspective that is not the body, but the “self”, which peers out through the face. The human face is the social instrument of persons. In seeking to understand you, or adjust how the world or your experience seems to you, I interact with you through your embodied perspective.

In pain experience, it is my loss of personal control over my body, and its dominion over me, that create the compelling sense, for me and for others, of an “incarnate” person. Pain imposes a significant vulnerability on persons: the vulnerability of a free person who is overwhelmed in his or her body by the presence of pain. This can make the person, and the person’s significant others, feel answerable for what he or she experiences.

Challenges facing pain reductionism

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The official scientific definition of pain was initially formulated in the 1980s by a committee organized by the International Association for the Study of Pain (IASP). This definition was updated in the 1990s by the IASP to reflect advancements in pain science and has since been widely accepted by the scientific community:

Pain: An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

Note:The inability to communicate verbally does not negate the possibility that an individual is experiencing pain and is in need of appropriate pain-relieving treatment. Pain is always subjective. Each individual learns the application of the word through experiences related to injury in early life. Biologists recognize that those stimuli which cause pain are liable to damage tissue. Accordingly, pain is that experience we associate with actual or potential tissue damage. It is unquestionably a sensation in a part or parts of the body, but it is also always unpleasant and therefore also an emotional experience. Experiences which resemble pain but are not unpleasant, e.g., pricking, should not be called pain. Unpleasant abnormal experiences (dysesthesias) may also be pain but are not necessarily so because, subjectively, they may not have the usual sensory qualities of pain. Many people report pain in the absence of tissue damage or any likely pathophysiological cause; usually this happens for psychological reasons. There is usually no way to distinguish their experience from that due to tissue damage if we take the subjective report. If they regard their experience as pain, and if they report it in the same ways as pain caused by tissue damage, it should be accepted as pain. This definition avoids tying pain to the stimulus. Activity induced in the nociceptor and nociceptive pathways by a noxious stimulus is not pain, which is always a psychological state, even though we may well appreciate that pain most often has a proximate physical cause (IASP-Task-Force-On-Taxonomy, 1994: 207-213).

An apparent immediate and inconvenient fact facing pain reductionism is that pain stubbornly resists identification with only the brain. The original pain identity statement, ‘Pain = C-fibre activation’ (Place, 1956), neglects two essential features of pain observed in contemporary pain science: (1) Conscious awareness of wounding is multimodal and is correlated with integrated visual, kinaesthetic, and enteric sensory modalities in addition to noxious signalling (e.g., Chapman et al. 2008); (2) Wounding is typically part of overall bodily awareness that is correlated with multiple reciprocal nervous, endocrine and immune states (e.g., Chapman et al. 2008; Lyon et al. 2011; van Rysewyk, 2013; Vierck et al. 2010). Convergent lines of evidence demonstrate that wounding followed by pain is strongly correlated with endocrine and immune operations as well as sensory signaling that together exert an extensive non-neural impact. These operations interact and comprise a defensive stress response to wounding [1].

A consideration of the higher structures of the central nervous system (CNS) alone reveals an extraordinarily complex picture of pain. Unimodal functional brain imaging studies of nociceptive transmission, projection and processing show that signals of wounding reach higher CNS levels via the spinothalamic, spinohypothalamic, spinoreticularpathways (i.e., the paleospinothalamic tract) including the locus caeruleus (LC) and the solitary nucleus, spinopontoamygdaloid pathways, the periaqueductal gray (PAG), and the cerebellum (e.g., Burstein et al. 1991; Price, 2000). The thalamus (THA) projects to limbic areas including the insula and anterior cingulate, which have been identified with the integration of the emotional and motivational features of pain (Craig, 2002, 2003a, 2003b). Noradrenergic pathways from the LC project to these and other limbic structures. Accordingly, pain reveals extensive limbic, prefrontal and somatosensory cortical components. A meta-analysis of the literature described brain operations during pain as a complex network involving THA, primary and secondary somatosensory cortices (S1, S2), insula (INS), anterior cingulate (ACC), and prefrontal cortices (Apkarian et al. 2005). Thus, the brain engages in massive, distributed, parallel processing in response to noxious signaling.

The mechanisms of multimodal integration pose a formidable challenge for pain scientists. Hollis et al. (2004) examined how catecholaminergic neurons in the solitary nucleus integrate visceral and somatosensory information when peripheral inflammation is present. Pre-existing fatigue, nausea, intense physiological arousal, and a systemic inflammatory response induced by proinflammatory cytokines (e.g., Anderson, 2005; Eskandari et al. 2003) are all correlated with sensory signalling in the experience of pain. In addition to Craig (2002, 2003a, 2003b), an increasing number of studies have investigated the integration of information from multiple sensory modalities and central operations correlated with emotion and cognition in pain (e.g., Bie et al. 2011; Liu et al. 2011; Neugebauer et al. 2009). The more we are able to delineate the qualia of pain and map these experiences onto specific multimodal physical operations, the closer we come to identifying pain with those operations.

So, why has Place’s (1956) original pain identity statement survived in philosophy of mind? One reason is that the use of ‘C-fibre activation’ by identity philosophers is merely a placeholder for whatever the eventual mechanisms of nervous systems prove to be. We now know that wounding is identical to specific endocrine and immune operations in addition to sensory signaling. These operations interact and in concert comprise a defensive stress response to wounding. However, the purpose of calling it the identity theory of mind is to separate it from philosophical theories that identify mental states with states of immaterial souls or minds (dualism), abstract machine systems (functionalism), or those theories that reject the reality of mental states (eliminativism). It is not to make any substantive assumption about the sensory modality. This is why Place’s (1956) pain identity claim of C-fibre activation has survived, despite being explanatorily incomplete.

[1]In clinical settings, problems of acute and chronic pain do not easily conform to pain-brain type identities. The persistence of chronic pain as a major problem in medicine may indicate that identifying pain with the brain (‘pain in the brain’) has failed to inform clinicians toward curative interventions (e.g., Chapman et al. 2008).


Anderson, J. (2005). The inflammatory reflex-introduction. Journal of Internal Medicine, 257(2), 122-125.

Apkarian, A. V., Bushnell, M. C., Treede, R. D., & Zubieta, J. K. (2005). Human brain mechanisms of pain perception and regulation in health and disease. European Journal of Pain, 9(4), 463-463.

Bie, B., Brown, D. L., & Naguib, M. (2011). Synaptic plasticity and pain aversion. European Journal of Pharmacology, 667(1), 26-31.

Burstein, R., Dado, R. J., Cliffer, K. D., & Giesler, G. J. (1991). Physiological characterization of spinohypothalamic tract neurons in the lumbar enlargement of rats. Journal of Neurophysiology, 66(1), 261-284.

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Liu, C. C., Shi, C. Q., Franaszczuk, P. J., Crone, N. E., Schretlen, D., Ohara, S., & Lenz, F. A. (2011). Painful laser stimuli induce directed functional interactions within and between the human amygdala and hippocampus. Neuroscience, 178, 208-217.

Lyon, P., Cohen, M., & Quintner, J. (2011). An Evolutionary Stress‐Response Hypothesis for Chronic Widespread Pain (Fibromyalgia Syndrome). Pain Medicine, 12(8), 1167-1178.

Neugebauer, V., Galhardo, V., Maione, S., & Mackey, S. C. (2009). Forebrain pain mechanisms. Brain Research Reviews, 60(1), 226.

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van Rysewyk, S. (2013). Pain is Mechanism. Doctoral Dissertation, University of Tasmania.

Vierck, C. J., Green, M., & Yezierski, R. P. (2010). Pain as a stressor: effects of prior nociceptive stimulation on escape responding of rats to thermal stimulation. European Journal of Pain, 14(1), 11-16.