The Complex Reality of Pain 9780367353698, 9780429342981

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THE COMPLEX REALITY OF PAIN Jennifer Corns

The Complex Reality of Pain

This book employs contemporary philosophy, scientific research, and clinical reports to argue that pain, though real, is not an appropriate object of scientific generalisations or an appropriate target for medical intervention. Each pain experience is instead complex and idiosyncratic in a way which undermines scientific utility. In addition to contributing novel arguments and developing a novel position on the nature of pain, the book provides an interdisciplinary overview of dominant models of pain. The author lays the needed groundwork for improved models and targeted treatments at a time when pain science, pain medicine, and philosophy are explicitly searching for both and failing to find them. The Complex Reality of Pain will be of interest to a broad range of researchers and students, including those working in philosophy of mind, philosophy of science, cognitive science, neuroscience, medicine, health, cognitive and behavioural psychology, and pain science. Jennifer Corns is Lecturer in Philosophy at the University of Glasgow, UK. Her research focuses on pain, affect, suffering, and death. She is the editor of The Routledge Handbook of Philosophy of Pain (Routledge, 2017), and co-editor of Philosophy of Pain: Unpleasantness, Emotion, and Deviance (Routledge, 2018) and Philosophy of Suffering: Metaphysics, Value, and Normativity (Routledge, forthcoming).

Routledge Studies in Contemporary Philosophy

Critical Perspectives from Idealism and Pragmatism Edited by Paul Giladi Philosophical Investigations in New Media and Technologies Alberto Romele Owen Flanagan and Beyond Edited by Bongrae Seok Jaroslav Peregrin Michael McKinsey Foucault and the Corporate Government of the Public Cory Wimberly Edited by Clara Fischer and Áine Mahon Edited by Anders Nes with Timothy Chan Jennifer Corns For more information about this series, please visit: https://www.routledge. com/Routledge-Studies-in-Contemporary-Philosophy/book-series/SE0720

The Complex Reality of Pain

Jennifer Corns

First published 2020 by Routledge 52 Vanderbilt Avenue, New York, NY 10017 and by Routledge 2 Park Square, Milton Park, Abingdon, Oxon OX14 4RN Routledge is an imprint of the Taylor & Francis Group, an informa business © 2020 Taylor & Francis The right of Jennifer Corns to be identified as author of this work has been asserted by her in accordance with sections 77 and 78 of the Copyright, Designs and Patents Act 1988. All rights reserved. No part of this book may be reprinted or reproduced or utilised in any form or by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying and recording, or in any information storage or retrieval system, without permission in writing from the publishers. Trademark notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Library of Congress Cataloging-in-Publication Data A catalog record for this title has been requested ISBN: 978-0-367-35369-8 (hbk) ISBN: 978-0-429-34298-1 (ebk) Typeset in Sabon by codeMantra

For Himma, to whom it was long promised.

The most compelling challenge of pain is to help the patient who is suffering pain. —Melzack and Wall, The Challenge of Pain, 1988

Contents

Preface

ix

1

Introduction: Pain in Life, Science, and Medicine

1

2

The Need for Complexity: Rejecting the Orthodoxy of Simplicity

30

Mechanistic Explanations: How Complex Idiosyncrasy Undermines Them

84

3 4 5 6

Adopting Scientific Eliminativism: How Complex Idiosyncrasy Undermines Scientific Utility

141

Rejecting Traditional Eliminativism: Why Pain Is Still Real

174

Conclusion: Living with the Complex Reality of Pain

199

Index

215

Preface

While treatment interventions in response to pain reports have advanced considerably, my interest in pain was first engendered by my personal acquaintance with its limitations. My father suffers migraine headaches for which there is no clear explanation and no relief beyond that offered by strong narcotics—highly addictive, desperate interventions only sometimes knock out the migraine while reliably affecting wide swaths of other functioning. Twenty years ago, my mother was diagnosed with the fibromyalgia that she simply continues to manage. As a teenager, I had raging cluster headaches: blinding pain that would come without warning and leave me writhing in screaming agony. After tests which revealed no explanatory abnormalities, they eventually simply went away. In my life, as in most, pain has first and foremost been a practical problem. It was only in graduate school for philosophy that I began to realise that pain was also a theoretical problem. In particular, I became hooked intellectually through the tales of pain dissociation, as presented in Nikola Grahek’s classic Feeling in Pain and Being in Pain. What could pains be, I began to wonder, such that they included things as dramatically different as those associated with my raging headaches and those calmly reported by pain asymbolics? What, come to think of it, could pains be such that after centuries of study we still can’t find them (or their correlates) anywhere in the body? What could they be such that, unlike any other recognised medical problem, their only accepted valid marker for treatment was a person reporting it? The theoretical and practical problems of pain are not independent. They must be solved together. This shouldn’t be surprising. What may be surprising is that the tools of philosophy are well-suited to helping solve them. Over coffee at an interdisciplinary conference last year, a leader in the philosophy of pain asked me, “Why do you focus on treatment? Surely that’s a whole other set of problems”. Rather taken aback, I found it difficult to know how to answer. Confused, I responded, “But don’t you

x Preface care about whether your theory of pain is useful for treatment?” Blithely, he responded that he didn’t. This attitude is apparently common. Philosophers—perhaps contemporary analytic philosophers, in particular—are lamentably not often considered to have much to contribute to practical endeavours. This is perhaps unsurprising since they often don’t consider themselves to have a practical offering, much less an obligation to deliver one. I admit to being a contemporary analytic philosopher and nothing of a scientist or clinician, but my aims in understanding pain are nonetheless practical. The best attempt to characterise what philosophy does of which I am aware was offered by Wilfrid Sellars. According to Sellars, philosophy is the attempt to figure out how things, in the broadest possible sense, hang together, in the broadest possible sense. As a philosopher with a special interest in pain, I have accordingly sought to understand how pain hangs together with everything else in the broadest possible sense. Right from the beginning, adequately doing this has seemed to me to require integrating the many ways in which pain is understood across the many specialised theories and purposes which refer to pain, but also to harmoniously integrate these with the ways in which pain is understood in everyday life for our everyday purposes— the place where all specialised theorising rightly begins. Of the many areas of life in which pain is referenced, the management and treatment of pain is the specialised purposes for which it is most important that we get it right. Here, as in everyday life, pain matters not only theoretically but practically. A theory of pain which has no connection to the practical realities, difficulties, and challenges of pain as suffered by everyday people in everyday life, and pain as managed and treated in the clinic, is inadequate. Such a theory fails to illuminate the role that pain plays in how things, in the broadest possible sense, hang together, in the broadest possible sense. From this methodological perspective, ignoring the clinic when theorising about pain is not only likely to yield a theory with scant practical utility, but it is bad philosophy. Accordingly, a major theme of this book is that for pain, treatment is the crucible for theory. It is treatment, above all, for which our specialised theories of pain—from science, philosophy, or any other discipline— should be useful. While a philosopher, I’ve written the book with the explicit goal of making it accessible to anyone from any discipline. I am not at all sure that I’ve succeeded in this, but I’m grateful to discussion partners and readers of drafts from a wide range of fields who have helped me do it as well as I currently can. More generally, I am grateful to a great many people for helping me develop and express the ideas in this book. The present work is a substantially altered version of the PhD I wrote at CUNY (2011) under the

Preface  xi supervision of Jesse Prinz, to whom I remain grateful. The work benefitted enormously from discussions with people in the City University of New York Graduate Center’s mind and cognitive science community, including, especially, Pete Mandik, Myrto Mylopolous, David Pereplyotchik, and David Rosenthal. I am grateful to the amazing students at Mount Holyoke College, who, while I was a fellow there in 2012, interrogated that PhD thesis with me as part of a senior philosophy elective. Chapter 2 is substantially based on Corns, J. (2014). The inadequacy of unitary characterizations of pain. Philosophical Studies, 169(3), 355–378, and Chapter 5 is substantially based on Corns, J. (2016). Pain eliminativism: scientific and traditional. Synthese, 193(9), 2949–2971, both reprinted with permission from Springer. I am grateful to the participants in The Pain Project (2012) and The Value of Suffering Project (2013–2016), both funded by the Templeton Foundation and based in philosophy at the University of Glasgow with PIs David Bain and Michael Brady. These projects facilitated discussion with people from a range of disciplines that were critical for the evolution of my thinking and the current work. Without David and Michael, in particular, I cannot imagine where I or my research might be. I am grateful to multidisciplinary contributors to the Routledge Handbook of the Philosophy of Pain (2017), who bore with my invasive editorial interest to yield not only chapters which I hope are useful to others but exchanges which were extremely useful for me and my own work. Finally, in the roughly ten years that I have been researching pain, I have had some great friends, who have helped me both personally and professionally in ways that have contributed to the completion of this work. Beyond those already mentioned above, these especially include Ben Colburn, Sharisse Kanet, Charlotte Kent, Monique Whitaker, and my husband—the amazing Robert Cowan.

1

Introduction Pain in Life, Science, and Medicine

1.1 Pain in Everyday Life What is pain? The question might seem like an easy one to answer. Don’t we all know what pains are? If someone tells you they are in terrible pain, you aren’t puzzled about what they are telling you. They would rightly find it bizarre if you responded by asking, ‘Pain? What’s that?’. Pain is ubiquitous in our everyday lives. Unsurprisingly, we thus have a wide range of folk platitudes about it. Folk platitudes are those statements which we take to be obviously true in our everyday lives, and which we assume that roughly everyone—or, at least, roughly everyone with whom we interact in everyday life—also takes to be obviously true. Folk platitudes about pain are truly abundant, and we might think that these decisively settle all interesting questions about both its existence and nature. Consider just a few statements from our rich corpus of everyday, platitudinous wisdom about pain. Pains, we believe, are typically felt in a certain part of the body, and, we believe, something is typically wrong with that felt place. Pains are unpleasant and come in different degrees of intensity, such that some pains are worse than others. Pain, we furthermore take to be obvious, is something that it is appropriate to avoid. Other things being equal, we act to alleviate our pains and, other things being equal, it is wrong to cause them. We also, however, believe that we would be in serious trouble without pain. We believe that pain is useful in typically alerting us to things which are wrong with the places they are felt and, at least typically, that pain is useful in motivating us to do something about whatever is wrong. We take these statements, and many more, to be obviously true in the normal course of our everyday lives. We expect general agreement, with roughly everyone with whom we interact in our daily lives, that these statements are true. These platitudes about pain are part of our everyday, “folk” psychological, theory about our mental episodes—our everyday theory about what we think, feel, desire, and so on. And again, we might well think that this everyday theory, with its profundity of pain platitudes, is good

2 Introduction enough to settle all questions about the nature of pain. We might, that is, think that questions about the nature of pain are as trivial as the truth of the statements about pain which partly comprise our everyday psychological theory. While much about pain is obvious, it may not be obvious why further questions about pain’s nature—questions about what pain is and what it is not—are of any interest. While I’ll argue in this book that the success of our everyday theory is sufficient for us to accept the existence of pains as posited by that theory, and to continue to successfully and usefully refer to pains for our everyday purposes, that everyday theory nonetheless leaves some difficult questions about pain’s nature unanswered. To begin to see the limitations of our everyday theory, consider that it won’t clearly settle whether many episodes which are reported in everyday life are pains or not. When people take morphine, they report pains that they don’t mind. Some masochists report pains that they enjoy. Those suffering from some types of chronic pain conditions report pains in bodily locations where no damage can be found. Those suffering from phantom limb pain report pains in bodily parts of theirs that they simultaneously know they do not have. Are all of these nonetheless pains? Are there pains which we do not mind or even enjoy? Are there pains which are not correlated with any damage, and in body parts of ours that we do not have? Courting yet further controversy, consider whether unpleasant emotional episodes are pains. Are episodes of heartbreak, grief, loss, and rejection all pains? Are instances of these ever pains? The right answers to these questions, whatever they may be, are not folk platitudes. We might stress the controversy, from the point of view of our everyday theory, by asking whether the pains described in the previous paragraph are really pains. Is grief really pain? Is the pain I experience after taking morphine really pain? If the masochist enjoys the damage to her body, is she really in pain when she sincerely reports her enjoyable experience? Our everyday platitudes do not directly settle these questions. The answers are not trivial or obvious. Controversy in a wide range of cases like those just mentioned is to be expected. Our corpus of pain platitudes is so extensive that it is unsurprising that there are some cases for which some of these platitudes hold and others fail. Controversy may be expected to ensue across at least some of these cases. If some of our platitudes about pain are true about an episode reported as pain, and some of our other platitudes are false about that reported episode, then there is room for disagreement. These are disagreements that our everyday theory, by itself, cannot settle. Armed only with our everyday theory, then, we may at best be able to answer questions about the existence and nature of only paradigm cases. I’ll consider paradigmatic pains to be those things about which all of our folk platitudes about pain are true. I’ll consider paradigmatic non-pains

Introduction  3 to be those things that we take it to be obvious are not pains because so many of the folk platitudes about pain fail for them. My wedding ring is a paradigmatic non-pain; so many of our folk platitudes about pain are false of it that we would not expect anyone to think it was a pain. If someone declared that my wedding ring was a pain, we would think they were speaking metaphorically or were using the word ‘pain’ in an idiosyncratic way, i.e. to refer to something other than the referent of ‘pain’ as posited in our everyday theory. The ache in my hip, from working a bit too hard at the gym this morning, is a paradigmatic pain; all of our folk platitudes are true of it. At best, our everyday theory of pain can settle the question of the nature only of paradigmatic pains and paradigmatic non-pains: it can tell us when something is obviously pain and when something is obviously not pain, but it cannot tell us about non-obvious cases. Not all by itself. Indeed, our everyday theory has some built-in limitations for decisively settling questions about which things are and are not pains. As above, we think that pains are typically felt to be in bodily locations and that there is typically something wrong with our bodies in those places that we feel the pain to be. Statements about what’s typical of pain are what I take to be obvious, and such statements are also what I take roughly everyone that I interact with to take to be obvious. But I do not assume general agreement that pains are essentially located, or that it is a necessary condition of pain that the body is damaged in the place the pain is felt to be. As us analytic philosophers might put it: everyday theory does not deliver the necessary and sufficient conditions for pain, nor does it identify the essence of pain. While I will return to this theme in later chapters, it is worth noting at the outset that I do not think that our everyday theory is intended for any such deliverances or appropriately evaluated by its deliverance of them. Our everyday theory is intended for our everyday purposes. As far as I can tell, there is no need for essences or necessary and sufficient conditions to accomplish these purposes. As Jerry Fodor might have put it: Granny gets along just fine without them. Statements which commit one to supposed essences or necessities, though often of interest to philosophers, are not statements that take place from within the grip of our everyday theory or that are required for the utility of that theory. The inability of our everyday theory to decisively determine the extension of its posits is not unique to pain. Our everyday theory may be deployed to yield a decisive ruling for paradigmatic cases of beliefs, for instance, and paradigmatic cases of non-beliefs. Taken on its own, however, it will not be able to settle questions about those episodes concerning which some platitudes about beliefs are true, while others are false. Similar considerations apply to desires, wishes, sensations, imaginings, and so on. Consider, for a single example, a belief sincerely reported by someone for whom that belief seems behaviourally inert across all

4 Introduction relevant circumstances. Or consider, for a second instance, a desire reported by someone who reports also believing that they wouldn’t like getting what they desired. These beliefs and desires may indeed be beliefs and desires, but they are not paradigmatic cases. To stress the controversy, we may ask whether they are really beliefs and desires. Does the person really want the thing that they believe that they wouldn’t like to have? Does a person really believe the thing they say they do, if that belief has no impact on any of their behaviour? In our everyday lives, we assume general agreement that beliefs affect behaviour in relevant circumstances, and we assume that we (at least) believe that we would like to have the things we desire. If beliefs and desires for which these platitudes fail are reported, we should expect disagreement about them. Our everyday theory could not settle these disagreements. Not all by itself. Further work needs to be done. Returning to pain: not only may our everyday theory fail to deliver a decisive ruling about what is and isn’t pain in all cases, but that theory gives rise to some particular puzzles about the nature of pain. While similar puzzles may arise for other of the posits of our everyday “folk” psychological theory, at least some of the particular puzzles which arise about the nature of pain are more particular to pain. One much-discussed puzzle about the nature of pain concerns whether pains are mental or extra-mental. We report pains as being located in our bodies: “there is a horrible pain in my foot”. As above, it’s a folk platitude that pains are (at least, typically) felt to be in bodily locations. This platitude, and others like it, suggests that pains are extended, extra-mental things located somewhere in our bodies. We also, however, report pains as being feelings of ours: “I took the aspirin, and my pain went away”. As above, it’s a folk platitude that pains are (at least, typically) feelings—nasty, unpleasant feelings (again: at least, typically). This suggests that pains are mental episodes which are located, if anywhere, in our brains or neural systems. If the doctor asks you where the pain is, you point to your foot; you don’t “point” to your mind. If the doctor asks you whether the pain is better, however, you introspect, i.e. you “look” inside your mind; you don’t look to your foot. This puzzle about what pain is—is it a mental episode or an extra-mental thing—arises from within our everyday theory, but it isn’t settled by it. While presumably no one thing, including pain, could be both mental and extra-mental (i.e. mental and not mental), our everyday theory of pain allows us to talk about pain as being both. We might settle this puzzle by privileging the platitudes according to which pains are one or the other. To again stress the controversy in everyday language: we might, that is, argue that pains are really in our bodies or, alternatively, argue that pains are really in our minds. Or, we might settle this puzzle by splitting up the platitudes and taking them to be true of two different, if somehow related, things. We might, that is, argue that the word ‘pain’,

Introduction  5 as deployed in our everyday theory, is ambiguous; our everyday theory posits pain_b, i.e. pains as extra-mental things in our bodies, and also distinctly posits pain_m, i.e. pains as mental episodes such as a feeling. Different philosophers have opted for all three (and further) of these responses.1 The point for present purposes is that settling which of these, if any, is the right resolution of the puzzle requires argument. Our everyday theory, by itself, does not settle the matter; in our everyday lives, we would not (and should not) assume general agreement about whether pains are really in our bodies, our minds, or both. Whichever way we solve this particular puzzle, were we limited to our everyday theory, yet further questions about the nature of pain would remain unanswered. If we opt for holding that pains are mental episodes, our everyday theory will nonetheless not settle questions concerning the kind of mental episode. Are pains sensations? Some of our folk platitudes seem to support this suggestion. Pains, I expect most everyone in my daily interactions to grant (at least typically), feel like something. They are, moreover, typically conscious and feel like something for someone to have—something, yet further, which is unpleasant or even awful for the one who has them (as ever: at least typically). Should we thus class pain with brute sensations, like a tingle or a red sensation? Or are pains instead perceptions? This alternative classification is likewise supported by some of our platitudes. I expect most anyone in my daily interactions to grant that pains are (again: at least typically) not only like something for one to have, but things which are about the extra-mental world of one’s body. “The pain of my toothache was much worse than the pain of my bruise”, I might say. Should we thus class pains with perceptions like seeing a red door or hearing a high-pitched bell? Even if we accept that pains aren’t brute sensations and accept that they are about something in the extra-mental world, perhaps they are nonetheless not best classed as perceptions. Perhaps a pain that is about, e.g., my foot doesn’t indicate anything about my foot but instead tells me to do something about my foot. Some platitudes may again here receive appeal. According to our folk platitudes, pains motivate us to do things. When in pain: we yank our feet from the fire, lick our chapped lips, and cradle our broken arms. Are pains, then, best classed as a kind of felt command? Thus, even limiting our understanding of pains to be mental episodes, our everyday theory cannot by itself settle questions about the kind of mental episode that pains are. Are pains sensations, perceptions, or imperatives? Are pains, instead, emotions or judgements of some kind? Though not discussed above, some platitudes likewise support accepting these alternative characterisations. Might each pain somehow be all of these things? Or might pains, as mental things posited by our everyday theory, sometimes be tokens of one type of mental episode and at other

6 Introduction times another, so that some pains are sensations, some are emotions, some are commands, and so on? Argument, here, is needed. Philosophers have attempted such arguments, and we’ll look at some of them in the following chapters. The point for present purposes is that our everyday theory, taken alone, does not settle the question of what type of mental episode pains may be; the relevant platitudes are promiscuous and not decisive. When going about our daily lives, we do not, and would not, expect general agreement about which of these kinds of episodes pains essentially or necessarily were—agreement, as we might put it, about what kind of mental episode pains really are. Were we to instead opt for holding that pains are extra-mental, our everyday theory again remains inconclusive for some further questions about pain’s nature. Are pains, taken as extra-mental things, simply any bodily disturbance? As we distinguish pains from, e.g., itch in our daily lives, this seems too permissive. In our everyday life, that is, we expect roughly everyone with whom we interact to agree that pains are not itches and itches are not pains. But what kind of more specific extra-mental, bodily thing might pains then be? Pains understood as extra-mental must be some kind of disturbance to the body, but what kind? Are pains damage to the tissue in our bodies? Or are they, instead, the signalling of any such damage? Or, for yet further options, are pains merely potential damage or the signalling thereof? Are pains, alternatively, the release of certain chemicals in our bodies, whether or not tissue is damaged or even “potentially” damaged? If so, which chemicals? While one may present reasons for or against any of these proposals, the folk platitudes alone will not settle it. While our everyday theory licenses my reporting “a pain in my foot”, that theory has little more to say about what particular type of extra-mental happening, if any, may be there occurring. Indeed, the poor correlation between pains as reported using our everyday theory and any identifiable extra-mental thing—broad or specific—has led most philosophers and all (to my knowledge) pain scientists and medical practitioners to distinguish pain from any bodily entity or activity. As discussed in later chapters, perhaps the best candidate for which type of extra-mental activity pain may be is nociception— the processing of high-threshold inputs via thermal, mechanical, and pressure receptors which are preferentially sensitive to such inputs, i.e. so-called nociceptors. But pain as reported and even nociception doubly dissociate: nociception frequently occurs without pain being reported or evinced in any other behaviours, and pain is frequently reported and evinced across many behaviours without the occurrence of nociception. 2 Notice that the lack of correlation between pain as reported and any identifiable extra-mental activity was of course a discovery garnered through specialised, scientific inquiry. It is not a folk platitude. The platitude that something is at least typically wrong in the bodily locations that we feel our pains to be might, on the contrary,

Introduction  7 have even suggested that the feeling of pain is well-correlated with some same, or at least similar, kind of bodily something on every occasion. For the present, the moral of the above considerations is that while our everyday “folk psychological” theory includes a profundity of pain platitudes that theory cannot by itself decisively settle questions about which things are and are not pains; whether pains are mental or extra-mental; or exactly what kind of mental or extra-mental things pains might be. For most of our everyday purposes, however, these limitations are unimportant. In our everyday life, we blithely refer to pains using all of the platitudes and do not expect everyone to agree about the best solutions to puzzles arising from the use of those platitudes or questions about the nature of pain which go beyond them. Disagreement reins when the puzzles or limitations are explicitly considered, and we do not assume agreement—beyond the platitudes themselves—in our daily lives. The utility of my everyday report for everyday purposes does not turn on whether pains are mental, extra-mental, or both. For everyday purposes, it does not matter whether we class pains as sensations, perceptions, bodily commands, emotions, or something besides. Matters of tissue damage, chemical signalling, or any other such extra-mental happening with which pains might be correlated, do not need to be settled. For our everyday purposes, we remain silent on these questions, blithely accept any puzzles about pain, and go along our merry (or not so merry) way— usefully referring to pains nonetheless. Indeed, the promiscuity of the notion may play an important part in facilitating the useful role in our everyday lives which the notion of pain patently plays. Pain is a posit of our everyday theory, and a contention running throughout this book is that pain is successfully and usefully referred to when we are engaged in the everyday purposes for which that theory has been developed. Despite the limitations of our everyday theory, some of which are built right in, we are nonetheless able to usefully and successfully refer to our pains when seeking aid, compassion, and comfort. Despite the limitations of our everyday theory, we are successfully and usefully able to identify paradigm instances of pain in ourselves and others. Perhaps precisely because of its promiscuity, our pain posit usefully encompasses a wide range of sensations, motivational profiles, attentional capture, significance, bodily involvement, evaluation, and more variation besides. Pains—as we refer to them in our everyday lives, for our everyday purposes, using our everyday theory—are a many-splendored (or perhaps better, many-deplored) thing. They vary, extensively, across persons and times. Our everyday theory not only tolerates but enshrines this complex variation. References to pain, however, are not limited to our everyday purposes: we refer to pain for a number of specialised purposes that have grown out of our everyday theory and everyday life. And while pain may be

8 Introduction successfully and usefully referenced for our everyday purposes, it does not simply follow from this that pains will be usefully referenced for all, or indeed any, of these more specialised purposes. In my everyday life, I successfully and usefully refer to trips to the museum, boring conversations, inappropriate adoration, and narrow-mindedness. It does not simply follow from this that any or all of these useful everyday referents are also usefully referenced for any or all of literary theory, gymnastics, physics, biology, chemistry, or any other specialised purpose. In this book, I’ll particularly focus on whether reference to pain—a posit of our everyday theory to which we successfully and usefully refer for our everyday purposes—is usefully referenced for the specialised purpose of science and medicine, broadly construed. There are, of course, other specialised purposes in which we are engaged that currently make reference to pain, e.g. literary theory, ethics, and theology. Though the discussion here may have implications for these, I will not explicitly consider them. The focus on science and medicine is motivated by concern about the treatment of pain. The medical purpose for which we refer to pain is, most centrally, its treatment. Moreover, as reflected in the development of pain science, the most important test for the utility of scientific generalisations about pain is their success in facilitating the treatment of pain when deployed within medical practice. It is treatment, above all, that our scientific generalisations about pain are intended to be useful for. Even if we accept that useful and successful reference to pain for either scientific or medical purposes doesn’t simply follow from whether reference to pain is useful or successful for everyday purposes, 3 it may nonetheless seem incredible that reference to pain is not useful for these. Pain science is burgeoning, and pain medicine is flourishing. A profundity of pain conditions is currently recognised in mainstream, Western medical practice—a practice which we take to be validated by scientific inquiry. Surely this all suggests that pain is appropriately investigated through scientific inquiry and targeted for treatment in medical practice. Doesn’t successfully treating pain require accepting that reference to pain is useful for medicine, and isn’t good medical practice facilitated by good scientific theorising? If so, isn’t it patently obvious that reference to pain within both scientific and medical practice is useful? Indeed, isn’t reference to pain crucial for these specialised purposes? On the contrary, I argue that pain is real, but complex and idiosyncratic such that it is (1) successfully and usefully referenced in everyday life, (2) it is not usefully referenced for scientific purposes, such that (3) the purposes of medical practice require using pain reports to identify non-pain targets for intervention. For Tuesdays, friendships, and a great many things to which we successfully refer in our everyday life, claims like these may be less controversial or interesting. It may, that is, not be very surprising that at least some things—things which really exist—are

Introduction  9 not usefully referenced for scientific purposes or targeted for medical practice.4 But these are certainly surprising claims about pain in life, science, and medicine—they were, at any rate, a great surprise to me—and it will take the rest of this book to explain and argue for them. In the rest of this chapter, I provide some background to help situate the arguments for these claims presented in the following chapters. First, I consider some ideas for thinking about when anything is usefully referenced for specialised scientific purposes (Section 1.2), followed by an initial overview of pain as currently referenced for both scientific and medical purposes (Section 1.3). I then provide a brief overview of the plan for the rest of the book (Section 1.4).

1.2 Natural Kinds and the Scientific Utility Criterion In focussing on whether pain is usefully referred to for scientific purposes, it’s helpful to briefly first consider the broader question of when anything from our everyday theory is usefully referenced for scientific purposes. Which of our everyday referring expressions would be usefully employed for scientific purposes? Which of the things to which we usefully refer in daily life are appropriate objects of scientific inquiry? Science is a kind of inquiry which trucks in generalisations, and there is a rich philosophical tradition focussed on illuminating the kinds of things about which science properly offers generalisations in the course of its inquiries. Those kinds of things into which science properly inquires are natural kinds, and the terms occurring in generalisations properly used to refer to such kinds are natural kind terms. There is no agreement, however, about how either natural kinds or natural kind terms are best identified and characterised. One might hold that natural kinds are those with essences, those which are projectable, and those which feature not only in generalisations but in laws of nature, or more besides. Any such account requires clarifying essences, projectibility, laws, or whatever. Valiant efforts are here ongoing. 5 In a pragmatic vein, however, I’ll stipulate that natural kinds are those that are usefully referenced in the generalisations of science—and, more specifically, usefully referenced for the explanations and predictions facilitated by those generalisations. It is worth noting that we humans make the generalisations and we use language to express them. The generalisations themselves don’t refer; we refer, using language. We use the word ‘pain’, for instance, canonically, to refer to pain. What we’re now considering is the utility of reference to pain, or anything else, when using scientific generalisations for explaining and predicting, i.e. for scientific purposes. Being referenced in generalisations is meant to limit extension to those things which are the subject of scientific inquiry. Being usefully referenced for explanation and prediction is intended to flag the function of scientific generalisations, i.e. to explain and predict. Beakers

10 Introduction and telescopes, for instance, presumably constitute kinds of things that are useful for scientific purposes without themselves being the object of the inquiry in the course of which they are used. We use beakers and telescopes to formulate generalisations which are useful for explaining and predicting things that are not themselves beakers and telescopes, though we might also submit beakers and telescopes to scientific inquiry. Note that this pragmatic stipulation is intended to be as liberal as possible; the more liberal the criterion, the harder it will be to show that a kind is not natural. I will proceed with this simple, liberal stipulation as the only appropriate criterion for a kind to be natural. Moreover, any term used to refer to such a kind is a natural-kind term. Once it has been determined that a kind and its term are earning, or are credibly expected to earn, their scientific keep, further disputes about whether the kind in question deserves the honorific title “natural” are no longer interesting, at least, for present purposes. For present purposes, the issue is whether a kind (whatever we call it) is usefully referenced for scientific theorising. Call this the scientific utility criterion.6 Using this criterion, to ask whether pain (or anything else) is usefully referenced for scientific purposes, is to ask whether pain (or anything else) is a natural kind (and vice versa). In answering this question for pain, I’ll focus most centrally on whether there is a pain mechanism or pain system, i.e. whether pain is subject to mechanistic explanation. While similar considerations arguably apply to any candidate natural kind, there are at least three good reasons to focus on mechanisms and mechanistic explanation in considering the scientific utility of reference to pain in particular. First, as will become clear in the following chapters, philosophers and pain scientists who hold that pain is a natural kind, i.e. it is usefully referred to for scientific purposes, apparently do so in virtue of an assumption that there is a pain mechanism or pain system. Much of the debate focusses on divergence in the identification and limning of the pain system and its function. The assumption that there is one, however, is broadly shared. If this seemingly widespread assumption is false, that should at least suggest the need for alternative, explicit reasons for thinking that pain is a natural kind. If there is no pain mechanism or system, that is, then some alternative reason will need to be given for thinking that reference to pain is useful not only for everyday life, but for scientific purposes. As discussed in the previous section, that reference is useful for scientific purposes doesn’t simply follow from there being useful reference for everyday purposes. Second, according to Richard Boyd’s (e.g. 1991, 1999) influential account, it is a necessary condition of natural kinds that they are subject to (homeostatic) mechanistic explanation. According to Boyd and his followers, natural kinds are those whose members have clusters of

Introduction  11 properties which usually co-occur as determined (i.e. as ‘brought about’) by an underlying homeostatic mechanism. Four conditions for a candidate kind to be natural can be liberated from the account (e.g. 1991): 1 2 3 4

Natural kinds have, and are identified by, clusters of usually cooccurring properties. Natural kinds have an underlying, homeostatic mechanism (that determines the cluster of usually co-occurring properties). Natural kinds feature in science’s generalisations, such that the referring terms in those generalisations refer to kinds that the correlative generalisations featuring those terms explain. Natural kinds are usefully referenced for explanation and induction (because of indicators 1–3), i.e. insofar as reference to a kind is not useful for induction and explanation, the kind is not natural.

Now I think that we do, indeed, identify pain by a cluster of co-occurring properties or features. This, I take it, is done through our everyday psychological theory, including its platitudes about pain, as described in the previous section. Pains are paradigmatically unpleasant sensations, felt to occur at a bodily location where there is damage, that motivate protective and avoidance behaviour; that we take to be bad for us; and so on—all as enshrined in our folk platitudes. If these features co-occur often enough (enough for us to say they ‘usually’ co-occur), then criteria 1 may be satisfied. Going further and focussing on mechanisms and mechanistic explanation for pain, however, will allow us to consider whether criterion 2, and in turn 4, are satisfied. These criteria are explicitly required on Boyd’s account. On this view, if there is no underlying mechanism—indeed, not just any old mechanism, but a homeostatic mechanism—which explains the co-occurrence of those co-occurring properties which we use to pick out a referent, then the corresponding referring expression is, at best, useful only for non-scientific purposes. Rather than a natural kind, we may have a “mere folk” conception. According to Boyd, the mere clustering of properties is insufficient to render a kind natural. References to such kinds for scientific purposes, Boyd maintains, will result in unacceptably unsuccessful scientific inductions and explanations. I do not here endorse Boyd’s account, but instead merely note that if we accept Boyd’s account, and there is no mechanistic explanation for pain, then we should reject the utility of pain for scientific inquiry. The current dominance and influence of Boyd’s theory is thus one reason to focus on mechanisms for pain when considering its utility for scientific inquiry. Third and finally, scientific inquiry arguably just is the search for mechanistic explanations. Such arguments are especially plausible for mental kinds. I will not actually attempt any such controversial arguments here,

12 Introduction but I note that this mechanistic take on the aim of scientific inquiry, for inquires of the mind in particular, is adopted by prominent theorists in philosophy of mind ranging from Hillary Putnam (e.g. 1967), Daniel Dennett (e.g. 1969), David Lewis (e.g. 1972), W.V. Quine (e.g. 1977), to William Bechtel (e.g. 2008). All hold that scientific inquiries into mental phenomena aim at mechanistic explanations. If this mechanistic understanding of the mental sciences is correct, then the only mental kinds that can fulfil the scientific utility criterion are those that will, ultimately, submit to a mechanistic explanation. Unless there is a pain mechanism, then pain—at least understood as a mental episode—is not an appropriate subject of scientific inquiry. To forestall an initial worry that specialists in theories of the mind may have, notice that this emphasis on mechanistic explanations is consistent with functionalism and multiple realisability. Functionalism, in various guises, is widely accepted as one of the best approaches to characterising the mind and its episodes. On a functionalist approach, mental episodes (e.g. beliefs, desires, emotions, and so on) are best characterised by their inputs, transitions to other mental episodes, and their outputs. Pains, on a functionalist view, would be characterised by the inputs to the episodes (e.g. getting punched) the transitions between pains and other mental episodes (e.g. becoming angry or concerned) and the outputs (e.g. rubbing the punched area or lashing out). Many functionalists, moreover, hold that functionally characterised kinds are multiply realised, which is to say that different physical systems, in different creatures, might all fulfil, or ‘realise’, the same (mental) functions. Thus, the realiser of the pain function in an adult human may differ from the realiser of the pain function in a frog, dog, or nonbiological organism. If accepted, multiple realisation may be thought to undermine the need to identify a single, underlying mechanism; a functionally characterised mental phenomenon may be explained by a multiplicity of mechanisms.7 We need to distinguish the idea that there is no mechanistic explanation of a phenomenon for a type of creature from the idea that there are many mechanistic explanations of a phenomenon within or across creature types. That a kind is realised by different mechanisms when realised by different organisms need not undermine the naturalness of a kind, i.e. the utility of reference for explanation and prediction when deployed in scientific generalisations. That a kind does not submit to a mechanistic explanation, even within a single type of organism, however, is another matter. Especially when one’s scientific generalisations are meant to range over all organisms of that type—as, one presumes, is the case with our mental sciences, e.g. psychology and neuroscience. On a mechanistic approach, we are aiming for mechanistic explanations of mental episodes for humans—this is consistent with different mechanisms realising functionally equivalent, or very similar, mental episodes

Introduction  13 for different creature types. As Putnam himself, a champion of multiple realisability, points out (1967, p. 163): …to investigate this [functional] hypothesis is just to attempt to produce ‘mechanical’ models of organisms—and is not this, in a sense, just what psychology is about? The difficult step, of course, will be to pass from models of specific organisms to a normal form for the psychological description of organisms. The claim that mental kinds were functionally characterisable and multiply realised was not intended to rule out the mechanistic explanations offered by scientific inquiry. Quite the contrary. Putnam, at least, was clear that the functional characterisation of a mental kind was intended as an important step in providing mechanistic explanations of it, while also allowing for different mechanistic explanations of a single phenomenon, differently realised. Similar considerations apply to the rather different type of functionalism championed by David Lewis. While the causal roles enshrined in the folk platitudes about a type of mental state may have various occupants in various kinds of creatures, there is presumed to be some one state that plays that causal role for (at least most of) the creatures in a population. Lewis requires that populations themselves are also natural kinds. Thus of pain and humans in particular, Lewis says (1980, p. 219): Human pain is the state that occupies the role of pain in humans… A state occupies a causal role for a population and the concept of occupant of that role applies to it, if and only if, with few exceptions, whenever a member of that population is in that state his being in that state has the sort of causes and effects given by the role. Putting aside the many differences between Putnam’s and Lewis’s functional characterisations of mental kinds, both types of functionalism leave open, indeed assume, that the “realisers” or “occupants” of functionally characterised kinds will be identified for a “type of organism” or “for a population”. And these are to receive mechanistic explanation. Functionalism is not in any conflict with the claim that we need a mechanistic explanation of a kind for reference to it to be useful for scientific inquiry—that is, for the kind to be natural. Functionalists may and often do adopt this mechanistic approach. Indeed, mechanisms and mechanistic explanation have been receiving renewed attention in the philosophies of mind and science. Stuart Glennan, William Bechtel, and Carl Craver are three prominent theorists in this area. On Glennan’s view, a mechanism is always defined for a behaviour, and “[a] mechanism for a behavior is a complex system that produces behavior by the interaction of a number of parts, where

14 Introduction the interactions between parts can be characterized by direct, invariant, change-relating generalizations”.8 According to Bechtel, similarly: “A mechanism is a structure performing a function in virtue of its component parts, component operations and their organization. The orchestrated functioning of the mechanism is responsible for one or more phenomena”.9 Finally, according to Craver: “Mechanisms are entities and activities organized such that they are productive of regular changes from start or set-up to finish or termination conditions”.10 In search of a working definition for present purposes, it is useful to emphasise the commonality among these accounts and ignore their differences. Accordingly, for present purposes, I’ll simply and liberally stipulate that mechanisms are wholes with parts that are organised and do things, such that the organisation and goings-on (interaction, operations, and activities) of the parts (entities) determines (produces, is responsible for, and are productive of) some behaviour or phenomenon of interest. As this definition is so broad, I’ll also use ‘mechanisms’ and ‘systems’ interchangeably. While we may offer distinct kinds of explanations, I’ll take a mechanistic explanation of a phenomena to be the successful identification of the mechanism whose organisation and goings-on determines it. Note again that these stipulations are intended to be as liberal as possible; the more liberal the criterion, the harder it will be to show that there is no pain mechanism or system, i.e. that pain is not only not mechanistically explained, but also not mechanistically explicable. To approach the question of whether pain is usefully referenced for scientific purposes, we might then first consider whether pain (our phenomenon of interest) is determined by the workings of some whole, with parts, that are organised and do things such that the organisation and goings-on of the parts determines pain. Is there a pain mechanism, or system, whose workings determine pain? Can we identify this mechanism and thus explain pain mechanistically? This is, again, a useful starting place for asking the question of whether pain is usefully referenced for scientific purposes for at least those three reasons given above. On some influential accounts of natural kinds and scientific inquiry of mental kinds, if there is no mechanism for pain, then the question of its naturalness is decisively settled in the negative. If our only reason for thinking that pain is usefully referred to for scientific purposes is that we assume that there is a pain mechanism, and there isn’t, then we need further reasons. If there is no mechanism which explains the co-occurring features by which we identify pain, then if we used Boyd’s criterion as necessary (and sufficient), pain would not be a natural kind. If scientific inquiry, of at least mental kinds, aims at mechanistic explanation, and there is (in principle) no such explanation for pain, then pain is not an appropriate subject of scientific inquiry (assuming that it is a mental phenomenon at all). I’ll take up the question of whether pain has a mechanistic explanation in Chapter 3, and

Introduction  15 I’ll there argue that neither pain nor any type of pain is mechanistically explicable. The interest in mechanisms and mechanistic explanation, however, is nonetheless derivative of our interest in the utility of reference to pain for the specialised purpose of science. As per the liberal scientific utility criterion, what most centrally matters is whether it is useful to refer to pain in scientific generalisations for explanation and prediction. And, I now stress, I want to grant that this may be so even if there is no pain mechanism or system, even if, that is to say, pain is not mechanistically explicable. If there is no pain mechanism, or system, for pain, then that is a strong reason to think that pain is not usefully referred to for scientific purposes. Strong, but not conclusive.11 As a final bit of simple, liberal, stipulation, I’ll consider pluralism about a kind to be the claim that despite mechanistic differences across the kind’s members, they nonetheless constitute a natural kind, since they are nonetheless usefully referenced using (at least some) generalisations of (at least some) relevant sciences for explanation and prediction. The lack of mechanistic explanation may be negligible for the utility of reference to a pluralistic kind. What matters is utility, and I want to leave open that a kind may be usefully referenced for scientific purposes, even if (and here I am more liberal than those theorists discussed above) it’s not mechanistically explicable. Again, the scientific utility criterion is intended to be as simple, liberal, and pragmatic as possible. If pain is usefully referenced for scientific purposes, then we should continue to refer to it for those purposes, even if there is no pain mechanism or system and even if there is no mechanistic explanation for pain. If mechanistic considerations aren’t decisive, however, then how can we tell? If pain isn’t mechanistically explicable, should we nonetheless accept pluralism for pain? In the case of pain, the specialised purposes of science are intertwined with those of medicine. It is, above all, the treatment of pain for which we should want our science of pain to be useful. I take the most important test for successful explanations and prediction in pain science to be effective treatment—both curative and palliative. This is true for mechanistic explanations as well: a good mechanistic explanation of pain should facilitate treatment. But it is also true for considering whether reference to pain within scientific generalisations is useful despite mechanistic failure. Medical practice is the key crucible for not only evaluating the adequacy of purported mechanistic explanations of pain but evaluating any candidate scientific generalisations about pain. The history of the science and medicine of pain reflects this. The science of pain has progressed and undergone dramatic transformation, almost entirely in the pursuit of improving medical practice. This is as it should be. The following section provides a brief history of these developments as relevant for present purposes.

16 Introduction

1.3 Pain in Science and Medicine Pain presents not only theoretical puzzles, but practical problems. Pains—as our folk platitudes enshrine—typically hurt. Pains can be unpleasant and downright awful. In extreme cases, suffering from prolonged pain can devastate our lives. As Cicely Saunders’s idea of ‘total pain’ suggests (e.g. 1976), some pain can seem to completely encompass a person. Any theory of pain needs to be informed by the crucial fact that real people suffer, sometimes terribly, from it. The theoretical challenges concerning the nature of pain addressed by philosophers and scientists are intertwined with the practical challenges of treating it which confront medical practitioners. Effective responses to pain will differ depending on what it is, and claims about what pain is are inadequate if they prove ineffective when tested in practice. As noted above, developments in the science of pain have thus rightly been motivated by a concern to understand the nature of pain in a way which will facilitate more effective treatment. Thus did the twentieth century witness a dramatic shift in the science of pain. After centuries of controversy, by around the second half of the twentieth, widespread agreement was being reached that pain was a simple sensation, i.e. a modality-specific sensation akin to any other modalityspecific sensation, e.g. colour sensations specific to vision. Though continuing to elude discovery, it was presumed that pain-specific receptors, pathways, and neural areas would all eventually be identified, i.e. we would eventually identify the presumed receptors, pathways, and neural areas dedicated specifically to pain sensation.12 Melzack and Wall’s gate-control theory (1965 and 1983), however, changed everything. They argued against both simplicity and specificity, identifying novel mechanisms that are often (though none always) involved in some (but none in all) pain experiences and identifying three dimensions of each token pain: sensory-discriminative, affective-motivational, and control processes— later dubbed the cognitive-evaluative dimension.13 These dimensions were explicitly identified not as mere causes or consequences of pain, but as genuine components. Phenomena previously considered to be merely causally connected to pain were now argued to be among its proper parts. The scientific community was persuaded, and the latter half of the century witnessed a shift to focussing upon multiple receptors, pathways, and neural areas—none now taken to be specific for pain. Despite other important differences, all dominant contemporary scientific models of pain now represent it as a multidimensional experience that paradigmatically includes sensation, affect, motivation, cognition, and evaluation. While further details will be discussed in Chapter 3, two points about the revolution in pain science that it heralded are worth initially emphasising. First, one consequence of the revolution is closer alignment with our everyday theory and pain platitudes. As already noted, in our everyday

Introduction  17 lives, we recognise that pains typically include a bodily sensation, the urge to do something in response to that sensation, an unpleasant feeling, the conviction that something bad is happening to us, and more besides. The shift in pain science away from the idea of pain as a simple and specific sensation, and towards a multidimensional experience with dissociating components, is one that I thus take to better respect the everyday theory from which the pain posit originates. In our everyday lives and interactions with others, we recognise that pains are a diverse class, and we accept that we experience—and, crucially, need treatment for—pains which vary greatly in their sensory, affective, motivational, cognitive, and evaluative aspects.14 Second, as discussed by Melzack and Wall, the revolution was explicitly motivated by the inadequacy of pain treatment. The wide range of pains reported by people seeking curative and palliative treatment, but which did not fit the dominant model of pain as a specific, simple sensation, were often simply presumed to be imagined, faked, or illusory. Regrettably, and despite the revolution, this continues to be the case far too often. In seeking to limn pain’s nature, it is important to remember that dubbing large swaths of pain as imagined, fake, or illusory has treatment implications for those that suffer them. Melzack and Wall’s revolutionary theory was explicitly motivated by the inadequate treatment those suffering from pain received as a result of the overly simplistic and narrow model then dominating. Again, for pain: treatment is the crucible for theory. Even as pain science has seen a revolution from specific, sensory models of pain to convergent, complex models, pain medicine has likewise been changing. Until recently, pain medicine—both research and diagnostics— almost exclusively employed a model of pain focussed on pathologies. According to this model, a patient presenting with pain is to be diagnosed such that the presumed pathological origin of their pain is identified and, if possible, eliminated. This approach is called the disease, or medical, model. While the medical model may strike one as obvious, or even inevitable, it has come under increasing scrutiny by many prominent pain scientists and medical practitioners. Smart et al. (2008) helpfully elaborates the traditional medical/disease approach and its problematic assumptions (p. 2): The medical/disease model refers to a tissue and pathology oriented approach towards the explanation of pain and dysfunction and functions on the premise that all pain has a dominant tissue or structural source. … The medical model is based on three broad assumptions: • There is a direct and proportional relationship between the amount of tissue damage and the level of pain experienced.

18 Introduction • There is a linear relationship between the amount of tissue injury and the degree of any ensuing physical impairment or disability. • Treating the pathology resolves the pain and therefore the disability. … [I]nterpretations and classifications of pain based on the medical/disease model and its structure-oriented approach have been criticized since such approaches do not explain the complexity and variability of pain presentations observed clinically; where pain is observed to persist after healing, where patients’ reports of pain in response to similar injuries differ greatly or where the magnitude of a pain report does not match the injury or pathology. Nor do they account for the variations in patients’ outcomes in response to interventions directed towards its treatment since by the tenants of the traditional medical model treatment of the pathological process should be accompanied by relief of pain. The motivation for the move away from the medical model is, I hope, clear. There are patients with the same pathology but varying pain, (at least) similar pains but varying pathologies, and pains with seemingly no pathology. We need, of course, to eliminate the pathologies, but we also need to eliminate the pain. Some sceptics of the medical model have accordingly begun turning, instead, towards a mechanism-based classification of pain.15 This alternative approach seeks to classify pains based on whatever underlying mechanism determines them and has been dubbed ‘pain analysis’. In a landmark editorial in Pain, Woolf et al. (1998) present the idea that the time in pain research had come when the medical/disease model should be replaced with a mechanism-based classification of pain that could, and should, be sought. As Woolf’s initial editorial forcefully argued, we need a characterisation of pain that will explain it more generally than the medical/disease model allows. Mechanisms were here assumed to be better able to fit this bill. Woolf urged the scientific community to look for general mechanisms responsible for pains whenever we find them—even, and especially, when they are not correlated with a disease, pathology, or tissue damage. Mechanisms could then serve as appropriate and effective targets for treatment interventions.16 From the beginning of the movement towards mechanism-based classifications of pain, including the influential 1998 editorial, different types of pain were hoped to be explained by what were already then recognised as different mechanisms. The reason is straightforward. Though there is disagreement about how pains should be grouped, if the groupings are to correspond to the workings of an underlying mechanism, then different types of pain are going to have to be grouped separately. Neuropathic pain and tissue injury pain, for an obvious instance, are known not to be determined or maintained by the same underlying  mechanisms.

Introduction  19 Woolf et  al. (1998), initially proposed three broad types of pain— transient pain, tissue injury pain, and nervous system injury pain—and corresponding possible mechanisms. For the latter two types, multiple possible mechanisms were identified (seven for tissue injury pain and eight for nervous system injury pain). Other, similarly rudimentary, mechanism-based classifications of pains followed.17 The new mechanism-based models thus do not seek to identify the pain mechanism; rather, they seek to identify various mechanisms explaining various types of pain. A mechanism-based classification of pain, while more general than disease or pathology-based classifications, will thus still require distinctions among pain types. For this reason, some pain scientists supporting a mechanism-based approach to pain suggest that mechanism-based classifications should be understood as a supplement to the traditional medical/disease model.18 Maybe some types of pains are explained by an underlying disease and pathology, such that elimination of that pathology eliminates the pain; perhaps “tissue-damage pain” is one such and should count as one among many types of pain. We’ll return to this sort of idea in Chapter 3. The key point for introductory purposes is that mechanism-based classification approaches were intended, from their inception, to eventually classify different types of pain by their correspondence with different explanatory mechanisms. To identify the mechanism determinant for instances of any pain type, both scientists and clinicians must use the symptoms and signs presented by patients. In particular, they must use patients’ reports. Here again, then, science and medicine are intertwined. As Finnerup and Jensen (2006, p. 110) point out, “Because patients report symptoms rather than mechanisms of pain, the main clinical problem is to extrapolate mechanisms from symptoms or clusters of symptoms”. The failed attempts to provide translations of symptoms and signs into mechanisms evidence the enormity of this problem.19 Even limiting the classification schema to distinct types of pain apparently leaves double dissociations between symptoms and any mechanisms proffered as candidates for explaining them. These problems are recognised by the mechanism-based advocates— and are recognised as being as yet intractable. These points are nicely summarised in Finnerup and Jensen’s (2006) critical analysis of extant mechanism-based classifications of neuropathic pain (p. 113): • •

To develop an effective mechanism-based classification, we need to be able to relate symptoms and signs to mechanisms and to identify specific treatments for specific mechanisms. One mechanism might give rise to different symptoms or signs; for example, upregulation of sodium channels in C-fibres increases fibre activity, resulting in burning pain, paroxysms, and dynamic mechanical allodynia.

20 Introduction • •

Similarly, one symptom or sign can be caused by several initiating mechanisms; for example, cold allodynia can be attributed to different mechanisms in peripheral and central neuropathic pain. It is becoming clear that we have not yet obtained a viable mechanismbased classification for neuropathic pain, and more rigorous studies are required to test this approach.

Note that this is a summary of the key points in a critical review of mechanism-based classifications of a particular type of pain— neuropathic pain. For that purported type of pain there are double dissociations between known mechanisms associated with neuropathic pain and neuropathic pain symptoms. The double dissociations between symptoms and signs and underlying mechanisms, even for particular pain types, are the largest problem facing the new movement towards a mechanism-based classification of pain. Whether or not we adopt a mechanism-based approach to replace the medical model of pain, the poor correlation between pain as reported and any currently specifiable activity in the body which undermines that model is now widely accepted across both pain science and pain medicine. And this poor correlation, which presents a theoretical problem for pain scientists, is a practical problem for medical practitioners. With or without bodily correlates, people arrive at the clinic, report pain, and require treatment. Despite currently lacking a mechanistic explanation for pain or pain types successful for intervention, and indeed lacking any valid biological marker for pain, medical practitioners still must act. The pressing need for treatment intervention in response to pain reports, despite the failures of our scientific generalisations and mechanistic models of pain, is reflected in the work of the International Association for the Study of Pain (IASP). The stated mission of the IASP is to “…bring together scientists, clinicians, health-care providers and policymakers to stimulate and support the study of pain and to translate that knowledge into improved pain relief worldwide”. 20 The IASP was founded in 1974 in the wake of the revolution in pain science and the recognition that too many seekers of pain relief were being dismissed on the grounds that their reported pains failed to conform to the simplistic scientific models of pain being revolutionarily rejected. In pursuit of their laudable goal of improved treatment, they offer a taxonomy of pain terms, explicitly claimed to be developed for use in clinical work. This taxonomy includes a definition for the term ‘pain’ itself. The IASP defines ‘pain’, that is the word, subjectively. According to the IASP, everything that is ‘reported as pain’ should be ‘accepted as pain’. We’ll consider the definition and its adequacy in greater detail in Chapter 4. But note now that the subjective pain report, emphasised by the IASP in its definition of pain, is not only the current gold standard for pain diagnostics, but it is now taken within medical practice to be

Introduction  21 the only valid marker for pain. Whether all medical practitioners consistently act accordingly or not, best practice is currently to accept all pain reports as veridical. If a patient says they are in pain, then they are in pain. As definitive of a medical condition, for use in clinical practice, a purely subjective definition is extraordinary. Imagine our surprise if the only accepted valid marker for any other medical condition, e.g. diabetes or cancer, was the subjective report. Imagine the absurdity of suggesting that the gold standard for diagnosing any other medical condition were patients’ reports that they had it, or that the patient report was the only valid indicator of the condition. It is understandable that the IASP has adopted this subjective criterion for pain, since all attempts at identifying a valid biological marker, even for specific types of pain, have failed. All we have left, this might suggest, is the report. If all that we have left for medical purposes is the report, then we have nothing left to target for medical intervention. The report is not the problem which the medical practitioner appropriately seeks to treat. It is, it seems to me, for this reason that Wall (1996), in defending the IASP definition, simply denies that a pain report is diagnostically useful; as per the IASP definition, the pain report is the only valid indicator of pain, but we should also—and perhaps for this very reason—deny that it identifies an appropriate treatment target. According to Wall, one of the clear leaders of modern pain science, a pain report is diagnostically inert.21 A pain report should, instead, be taken as an invitation to ask further questions which may then uncover an appropriate target. We treat the pain by identifying non-pain targets on which to intervene. The appropriate interventions for some pains are pharmaceuticals which target prostaglandin release (like aspirin) or the central nervous system (like morphine); for others it is non-pharmacological intervention which stimulates low-level receptors (like massage or TENS); for yet others it is appropriate to take no intervention whatever, and so on and so forth. The target for treatment intervention is a non-pain—even if intervention on that target, on some occasion, relieves the pain—since, as we have learned, any such specifiable targets are poorly correlated with pains as reported across persons and times. Whether or not we accept the IASP definition of pain, two things about the current situation in pain science and medicine bear introductory emphasis. First, pain reports do not identify appropriate targets for intervention. Of course, for characterising pain, we have more than simply the report: we also have all the platitudes of our everyday theory. As seen above, however, these too fail to be enough to specify treatment targets; the platitudes of our everyday theory, taken alone, do not even settle whether pains are mental or extramental, much less what kind of mental or extramental thing that pains might be and upon which we

22 Introduction might intervene for treatment. Our everyday notion of pain is simply too promiscuous for its report to identify an appropriate target for effective intervention. This much, at least, the IASP definition gets right. Though I’ll raise worries about the IASP definition of ‘pain’ (again: the word) in Chapter 4, the point for introductory purposes is that pain reports do not identify targets for intervention. Second, the medical practitioner must nonetheless intervene to treat in response to pain reports. Sufferers reporting pain often need treatment despite the fact that pain reports fail to identify treatment targets and we cannot translate the reports into any scientific generalisations which reliably do. As above, Wall thus recommends that we take the role of the pain report, in medical practice, to be a prompt to seek further information which may then identify a treatment target, i.e. identify something for which we have reliable scientific generalisations, e.g. prostaglandin release. In a similar vein, I suggest that the doctor must take the pain report in just the same way as they take any other report in everyday language which refers to our everyday posits. On this approach, the medical practitioner may be seen, in general, as a translator between our everyday theory—and the reports made from within that theory— and our specialised, scientific theories—and the appropriate treatment targets which they uncover. As pain science, however, has failed to yield any generalisations about pain which are successful for pain treatment, the pain report is thus appropriately translated into identification of a non-pain target for intervention, e.g. prostaglandin release, central nervous system functioning, or low-level receptors. We’ll keep the clinician firmly in mind throughout and briefly return explicitly to the idea that they are translators in the concluding Chapter 6. Might pain science eventually do better? Might we eventually identify adequate mechanistic explanations for pain, or, at least, for types of pain, such that we can target those mechanisms for treatment interventions? And, even if no mechanistic explanations are forthcoming, even in principle, might we nonetheless identify scientific generalisations which successfully explain and predict pain? Perhaps our pain science simply needs to advance. Especially if we are naturalists, we might assume that scientific generalisations about pain and pain types which are successful for explaining and predicting pain must—at least eventually—be in the offing. While further evidence might convince us otherwise, I argue in Chapter 4 that pain science, as tested by the crucible of pain medicine, has revealed pain to be a complex, convergent, and idiosyncratic mental episode that is successfully and usefully referenced for everyday purposes, but which is not usefully generalised about for any scientific purposes. Pain, as an analytic philosopher like I might put it, is real, but it is not natural. If we take medicine to fall within the purview of science, we may take this to entail that pain is not usefully referenced for medical purposes. As hinted above, however, I’ll instead take medical purposes

Introduction  23 to include the translation of pain reports in everyday language into identifications of mechanistically explicable non-pain targets for intervention. This is, I take it, a general feature of medical practice not limited to pain medicine. Insofar as medical practice lies at the interface of everyday theory and specialised, scientific theories, we may take all the posits of both everyday theory and the relevant scientific theories to fall within its purview. Listening, understanding, and adequately responding to reports given by patients using everyday theory is a critical skill for those medical practitioners engaging the everyday public in the clinic. Medical practice requires the deft use of scientific generalisations, along with careful attention to the complex idiosyncratic realities of the biological, psychological, and social situations of their patients. Would accepting the complex idiosyncratic reality of pain be problematic for treatment? On the contrary, it is my hope that more accurately recognising pain for what it is and what it is not will improve treatment. Rather than attempt to shoehorn all pains into an overly simplified, onesize-fits-all model—and dismissing all those not captured by the errant model as mere illusions, delusions, confusions, or worse—the current proposal allows us to recognise the complex idiosyncrasy of pain not only in our everyday lives, but in the clinic. As each pain, like each person, is idiosyncratic, so also are the appropriate responses to each person’s pain. This is something we recognise in everyday life. For a headache reported using the same or very similar terms: I bring my mother a cup of peppermint tea, my husband a paracetamol, my father-in-law a whisky, and my best friend a martini. As evidenced not only by the IASP definition of pain, but by biopsychosocial models of pain, 22 the rise of the pain clinic, and the concept of ‘total pain’ in end of life care, 23 pain medicine is already shifting from the assumption of pain as a biological, chemical, or mechanistic phenomenon— explanatory and predictive scientific generalisations about which hold across persons and times—to an understanding of pain as an idiosyncratic, complex experience whose appropriate treatment interventions differ from case to case. This book is intended to be a contribution to that shift.

1.4 Preview of Remaining Chapters So, what is pain? Pain is a posit of our everyday theory, best characterised in the boring and loose way which that theory says, i.e. using all the folk platitudes with which I began this introduction and many more which space precludes mentioning. Pains, characterised as such, are usefully and successfully referenced for everyday purposes. Our everyday theory respects the complex idiosyncrasy of pains. In everyday life, we accept the myriad ways that pains differ across persons, times, and creatures.

24 Introduction As the core positive proposal is that pains are best characterised in the loose way that we characterise them for everyday purposes, much of this book is most centrally focussed on arguing against the attempts from philosophy and science to unjustifiably narrow our understanding of pain. While the motivations for this narrowing are most always laudable, the consequences—in particular, the consequences for the treatment of pain—are lamentable. In arguing against these oversimplifications, I will thus often be focussed on what pains are not. More specifically, I’ll argue that pains, though real, are nonetheless not usefully referenced for scientific purposes. The broad and diverse class of things that our everyday theory allows to be pains are determined by the idiosyncratic convergence of distinct sets of multiple mechanisms on distinct occasions. Pains are real, but they are complex and idiosyncratic in a way which undermines useful generalisations about them for scientific purposes. Neither pain nor any type of pain is a natural kind. The complex reality of pain, as posited in our everyday life, and the lack of utility in referencing it for scientific purposes, has implications for medical practice. People arrive at the clinic and report their circumstances using everyday theory—that is, they will reference posits, including pain, from everyday theory. Medical practitioners seek to provide diagnoses and identify treatment targets for interventions as validated through scientific inquiry. If the arguments here are correct, then while achieving the goals of medicine requires taking patient pain reports seriously, it also requires identifying exclusively non-pain targets for treatment intervention. The remainder of the book argues for these claims and their implications. I begin in Chapter 2 by focussing on the contemporary accounts of the nature of pain currently dominating analytic philosophy. The starting point for such theories is a view which I dub the orthodoxy of simplicity. According to this orthodoxy, pains are mental episodes which are pains in virtue of their distinctive qualitative character, i.e. in virtue of what it is like for one to undergo the mental episode (at least, when that episode is conscious). I dub this qualitative character the pain quality. Much of contemporary, analytic philosophy of pain has focussed on debating which theory of qualitative character best accounts for the pain quality. Pain has thus been used as something of a test case for accounts of qualitative character. While I offer some general considerations against the orthodoxy of simplicity, my central strategy for arguing against it is to reverse this line of thought. Drawing on pain reports from everyday life and clinical observations, I argue that granting the dominant, contemporary theories of qualitative character and applying these to the supposed pain quality, none is necessary or sufficient for pain: there is an undermining glut of dissociations between pain and any distinctive pain quality as understood by these theories. If someone is firmly committed

Introduction  25 to one of these theories of qualitative character, they should reject the orthodoxy of simplicity. The central strategy deployed for most of Chapter 2 is admittedly limited. One might think that all that the arguments given there show is that we are still lacking an adequate account of qualitative character—not that we should reject the orthodoxy of simplicity. While I argue that the orthodoxy is unmotivated and unsupported by everyday life, medical practice, or pain science, and—indeed—would require major revision to our everyday theory, one might nonetheless think that pain science might yet somehow vindicate the orthodoxy by identifying a pain system whose working corresponds with the supposedly distinctive pain quality. I thus directly turn, in Chapters 3 and 4, to the science of pain. In Chapter 3, as previewed above, I show in more detail how pain science has come into greater alignment with everyday theory in recognising pain to be a multidimensional experience that paradigmatically includes sensation, perception, emotion, cognition, and motivational responses. This multidimensionality is enshrined in all leading scientific models of pain. I argue, however, that none of these models identify a mechanism (neurobiological or otherwise) which adequately explains pain. While this may be taken to simply suggest that further work needs to be done, considering extant research on pain types reveals that some mechanisms are involved in some pains and not others. At best, we might arrive at distinct mechanistic explanations of distinct types of pains. Recent work in pain science which attempts to provide mechanism-based classifications and explanations of pain types, and their admitted failures thus far, here prove instructive. What they are finding, in short, is that not only do different pain types involve distinct mechanisms, but that each token pain results from the convergent activation of multiple mechanisms—genetic, chemical, biological, social, and more. And the convergence of the activity of these multiple mechanisms is highly idiosyncratic. This idiosyncrasy is crucial for explaining pain tokens, but it blocks successful mechanistic explanations about pain types or pain as such. It is then what we already know about the mechanisms implicated in token pains which allow us to conclude against any eventual mechanistic explanations of pain types. I’ll conclude that neither pain nor any pain type will submit to mechanistic explanation. The overall moral of Chapter 3 is that each token pain—as revealed by scientific inquiry—is determined by the idiosyncratic convergence of the activity of multiple mechanisms. Put a bit less technically: the mechanistic activities which determine any particular pain vary from person to person, and indeed for the same person across times. Call this the complex idiosyncrasy of pain. Chapter 4 focusses on whether pains may be usefully referenced using scientific generalisations for explanation and prediction despite lacking

26 Introduction mechanistic explanation. That is, recall, whether we should accept pluralism for pain. Drawing on the complex idiosyncrasy of pain, I argue against pluralism and in favour of eliminating references to pain from pain science, i.e. for a position called scientific eliminativism. By drawing on actual cases from the clinic and considering the IASP definition of pain, I argue that no utility will be lost by eliminating reference to pains for scientific inquiry, as long as references to the non-pain mechanisms, uncovered by inquiries in search of improved pain treatment, are retained. In short, the complex idiosyncrasy of pain undermines useful scientific generalisations about pain. More technically put: neither pain nor any type of pain is natural kind. In Chapter 5, I argue that despite the fact that the scientific utility of reference to pain is undermined by their complex idiosyncrasy, they are nonetheless real. Those of us who are naturalistically inclined might think this problematic; we might think that anything not usefully referenced within scientific inquiry simply doesn’t exist at all. Scientific inquiry, we might think, is not merely a specialised purpose among others, but the method by which we can and should definitively settle questions of existence. If we cannot have successful scientific generalisations about pains, then there must not be any pains. Against this, I argue that the references to pain in everyday life are sometimes successful and useful and should accordingly be retained. Contrary to some traditional eliminativists about pain, our everyday notion of pain is neither irresolvably contradictory nor problematically simplistic. Crucially, the idiosyncratic complexity of pain, which subverts the utility of scientific generalisations, does not disrupt utile reference in everyday life. Neither does idiosyncrasy entail non-existence nor any nonphysical substances. Pain may thus serve as a case study of a real and robust kind posted by our everyday theory, which is nonetheless not a natural kind. In Chapter 6, I conclude with some reflections of the implications of the previous chapters. There are implications not only for philosophical theorising about pain but for general implications concerning naturalism and our everyday ‘folk’ theory. Crucially, there are also implications for pain medicine. Like the philosopher, the medical practitioner works at the interface of theories developed for distinct purposes in pursuit of their own. Like the philosopher, and as previewed above, the medical practitioner must work as a translator between multiple theories which may each usefully reference distinct posits. I conclude on the hopeful note that the management and treatment of pain may continue to improve as we reject all attempts to oversimplify it and increasingly recognise the extent of its complexity and idiosyncrasy. Recognising the reality of complex and idiosyncratic episodes is not only useful but crucial for everyday life, wherein our complex idiosyncrasy

Introduction  27 as persons is and should be paramount. Science shows no partiality and is no respecter of persons. This is as it should be. For medical practice, however, as for everyday life, we must nevertheless continue to care about individual people and to recognise the real, complex, and idiosyncratic pains from which they suffer.

Notes



20 See: www.iasp-pain.org/Mission?navItemNumber=586. 22 See for instance Flor and Hermann (2004). 23 See Clark (1999) for discussion.

28 Introduction

References Arner, S. (1998). Pain analysis in prediction of treatment outcome. Acta Anaesthesiologica Scandinavica, 42, 24–28. Bechtel, W. (2008). Mental mechanisms: Philosophical perspectives on cognitive neuroscience. Taylor & Francis. Bechtel, W., & Abrahamsen, A. (2005). Explanation: A mechanist alternative. Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences, 36(2), 421–441. Bechtel, W., & Richardson, R. C. (2010). Discovering complexity: Decomposition and localization as strategies in scientific research. MIT Press. Boyd, R. (1991). Realism, anti-foundationalism and the enthusiasm for natural kinds. Philosophical Studies, 61(1–2), 127–148. Boyd, R. (1999). Kinds, complexity and multiple realization. Philosophical Studies, 95(1–2), 67–98. Clark, D. (1999). Total pain’, disciplinary power and the body in the work of Cicely Saunders, 1958–1967. Social Science & Medicine, 49(6), 727–736. Corns, J. (2012). Pain is not a natural kind. City University of New York. Corns, J. (Ed.). (2017). The Routledge handbook of philosophy of pain. Taylor & Francis. Craver, C. F. (2006). When mechanistic models explain. Synthese, 153(3), 355–376. Craver, C. F. (2007). Explaining the brain: Mechanisms and the mosaic unity of neuroscience. Oxford University Press. Dallenbach, K. M. (1939). Pain: History and present status. The American Journal of Psychology, 52(3), 331–347. Dennett, D. C. (1969). Content and consciousness. Routledge. Finnerup, N. B., & Jensen, T. S. (2006). Mechanisms of disease: Mechanismbased classification of neuropathic pain—A critical analysis. Nature Reviews Neurology, 2(2), 107. Flor, H., & Hermann, C. (2004). Biopsychosocial models of pain. Progress in Pain Research and Management, 27, 47–78. Gifford, L. S., & Butler, D. S. (1997). The integration of pain sciences into clinical practice. Journal of Hand Therapy, 10(2), 86–95. Glennan, S. (2002). Rethinking mechanistic explanation. Philosophy of Science, 69(S3), S342–S353. Glennan, S. (2005). Modeling mechanisms. Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences, 36(2), 443–464. Hawley, K., & Bird, A. (2011). What are natural kinds? Philosophical Perspectives, 25(1), 205–221. Jensen, T. S., & Baron, R. (2003). Translation of symptoms and signs into mechanisms in neuropathic pain. Pain, 102(1), 1–8. Khalidi, M. A. (2013). Natural categories and human kinds: Classification in the natural and social sciences. Cambridge University Press. Lewis, D. (1972). Psychophysical and theoretical identifications. Australasian Journal of Philosophy, 50(3), 249–258. Lewis, D. (1980). Mad pain and Martian pain. Readings in the Philosophy of Psychology, 1, 216–222.

Introduction  29 Machamer, P., Darden, L., & Craver, C. F. (2000). Thinking about mechanisms. Philosophy of Science, 67(1), 1–25. Melzack, R., & Casey, K. L. (1968). Sensory, motivational, and central control of determinants of pain. The skin senses, 1, 423. Melzack, R., & Wall, P. D. (1965). Pain mechanisms: A new theory. Science, 150(3699), 971–979. Melzack, R., & Wall, P. D. (1983). The challenge of pain. Penguin Books. Putnam, H. (1967). Psychological predicates. Art, Mind, and Religion, 1, 37–48. Quine, W. V. (1977). Naming, Necessity, and Natural Kinds, edited by S. P. Schwartz. Ithaca and London: Cornell University Press. Saunders, C. (1976). Care of the dying–4: Control of pain in terminal cancer. Nursing Times, 72(29), 1133–1135. Smart, K. M., O’Connell, N. E., & Doody, C. (2008). Towards a mechanismsbased classification of pain in musculoskeletal physiotherapy? Physical Therapy Reviews, 13(1), 1–10. Wall, P. D. (1996). Response to editorial by Anand and Craig. Pain, 67(1), 209. Woolf, C. J. (2004). Pain: Moving from symptom control toward mechanismspecific pharmacologic management. Annals of Internal Medicine, 140(6), 441–451. Woolf, C. J., Bennett, G. J., Doherty, M., Dubner, R., Kidd, B., Koltzenburg, M., & Torebjork, E. (1998). Towards a mechanism-based classification of pain? Pain, 77(3), 227–229.

2

The Need for Complexity Rejecting the Orthodoxy of Simplicity

2.1 Enter Analytic Philosophy Our everyday theory of pain, as we’ve seen, does not—by itself—offer answers to all questions about the nature of pain. Disagreement between people in non-paradigmatic cases is to be expected in our everyday life. Our everyday theory does not alone settle whether pains are mental episodes or non-mental entities, what kind of either, both, or neither. And, as we’ve seen, it raises puzzles about pain that the theory alone cannot solve. Enter analytic philosophy. Analytic philosophers of pain seek to offer an account of pain that solves the puzzles of everyday theory and yields a decisive verdict on whether any candidate entity is or is not a pain. To do this, they typically seek to identify the necessary and sufficient conditions of pain, i.e. what is necessary for something to be a pain and what is sufficient for something to be a pain. Going further, they may seek to offer an account of the supposed essence of pain.1 Though some take our everyday notion to be ambiguous between two distinct notions of pain—one as of a mental episode and one as of a bodily, non-mental entity2 —others take pains to be bodily, non-mental entities, 3 while still and most others take them to be mental episodes. The dominant contemporary, analytic philosophical view is that pains are mental episodes with a distinctive qualitative character. To be in pain, according to such views, is to undergo a mental episode that—at least when conscious—it is like something for you to have. And what’s it like for you? Well, it’s pain! There is, as we might put it, a distinctive qualitative way that mental episodes which are thereby pains feel. It is being that qualitative way, it is feeling like that, which makes a mental episode a pain. I’ll dub this supposedly distinctive qualitative character that mental episodes which are all pains have, and in virtue of which they are supposedly pains, the pain quality. Though the position is by no means original to him, Saul Kripke’s (1980) Naming and Necessity Lectures may be taken as providing one contemporary presentation of the view that pains are all and only those mental episodes which have the pain quality. According to Kripke, pain

The Need for Complexity  31 just is its “immediate phenomenological quality”. Terminology here is torturous, but we may take ‘phenomenological quality’ to be conscious qualitative character, i.e. what it’s like for one to undergo a mental episode, when that mental episode is conscious. He says (pp. 152–153, italics added): Pain… is not picked out by one of its accidental properties; rather it is picked out by the property of being pain itself, by its immediate phenomenological quality. … Thus it is not possible to say that although pain is necessarily identical with a certain physical state, a certain phenomenon can be picked out in the same way we pick out pain without being correlated with that physical state. If any phenomenon is picked out in exactly the same way that we pick out pain, then that phenomenon is pain. While doubts can and have been raised about much of Kripke’s discussion, of central interest for present purposes is the claim of Kripke’s that is accepted by dominant, contemporary, analytic philosophical theories of pain: namely, that there is a distinctive qualitative character in virtue of which a mental episode is a pain, i.e. the pain quality. Unlike Kripke, most contemporary philosophers of pain dominating the conversation are naturalists, holding that the right account of the pain quality is to be at least informed by scientific inquiry. But that there is some such distinctive qualitative character, and that pains are all and only those mental episodes which have it—however we identify the episode and whether it is identical to any physical state—is taken for granted by the dominant theorists of pain in analytic philosophy. I dub this view the orthodoxy of simplicity. While the account of the pain quality itself may be complex, the claim that mental episodes are pains in virtue of having a distinctive qualitative character—the pain quality—is simple. On this orthodox position, there is ultimately a simple explanation of pains: they are those mental episodes with a distinctive qualitative character, i.e. those that have the pain quality. Much of contemporary, analytic philosophy of pain has proceeded from this starting point and accordingly been aimed at identifying the right account of the pain quality. Indeed, pain—understood in accordance with the orthodoxy of simplicity—has come to prominence in philosophy as a test case for theories of qualitative character in general. Against the background assumption that there is a distinctive pain quality, a theory of mental qualities is tested by its ability to account for it. The standard wisdom is that an adequate theory of qualitative character must account for the pain quality. Before considering leading attempts to account for this supposed quality, it is worth first considering why we should accept this starting point: why accept that there is a distinctive, qualitative character in virtue of which a

32  The Need for Complexity mental episode is a pain? I’m unaware of any arguments for this claim actually being given in the literature. I presume that it is supposed to be obvious. Kripke (1980) certainly takes it to be obvious throughout, at one point rhetorically asking (146), ‘Can any case of essence be more obvious…?’ The orthodoxy of simplicity has not been questioned but is instead a place where most contemporary, analytic philosophical theorising begins. In the following section, we’ll consider what reason we might give in favour of the orthodoxy of simplicity and, in particular, whether it is supported by introspection. Whether, that is, the way our pain experiences seem to us, from the inside, supports the orthodox view. It will be important, when introspecting, to be careful to distinguish the supposed pain quality from other qualities. Unsurprisingly, reports are likely to differ. Introspective claims are limited. Often, it seems, we find our experiences to be just as we expected to find them. In the rest of the chapter, I deploy a strategy against the orthodoxy of simplicity that reverses the standard line of thought: rather than using the pain quality to test theories of pain, I’ll grant the dominant theories of the supposed pain quality on offer and consider whether they adequately account for pain. Both currently dominant theories of the pain quality are intentional accounts. According to these theories, qualitative character is to be explained by intentional content—a notion below explained. In Section 2.3, I consider the intentionalist, representational content account of pain, and in Section 2.4, the intentionalist, imperatival content account. I argue that both are inadequate. For reasons that will become clear, one may think that identification of a distinctive pain system may yet vindicate an intenitonalist account of pain or, alternatively, that the workings of such a system may explain the supposed pain quality without the need to appeal to any distinctive intentional content.4 More generally, one may think that the arguments in Sections 2.3–2.4 merely show that we still just need a better theory of qualitative character which can vindicate the orthodoxy of simplicity. Section 2.5 thus concludes the chapter by offering some general considerations against the supposed pain quality which again leads us to considerations of a supposed pain system which may yet vindicate the orthodoxy. Is there such a pain mechanism or system? In the following chapter, we turn directly to the science of pain, where I’ll argue that pain science itself has revealed that there is not.

2.2 The Orthodoxy of Simplicity Why accept the orthodoxy of simplicity? Why accept that pains are all and only those mental episodes with a distinctive qualitative character, i.e. those episodes that have the pain quality? As above, I’m not aware of any reasons being explicitly given for the orthodoxy, but I presume that at least one supporting reason—perhaps

The Need for Complexity  33 even the supporting reason intended to be decisive— is supposed to be introspection. It is introspection which makes the orthodoxy obvious. When we consider our mental episodes ‘from the inside’, as we might put it, we are supposed to find that all and only those mental episodes we take to be pains have the pain quality. All of our pains feel like pains. With Kripke above, we might go further and think that pain just is anything which I introspect and find to have the pain quality. Consider the following claim: INTROSPECTION: Whenever I introspect my pain experiences, I find a distinctive, qualitative character—a ‘what it is like for me’—that is common to them all. I want to be clear, right upfront, that when I introspect my own pain experiences, I find no such qualitative character. This is not, as far as I can tell, an artefact of my specialised theorising: I have found the assumption that there is such a quality bizarre since beginning my pain research. On the contrary, it seems to me that pains, prima facie—i.e. on the face of it—vary widely in their qualities. Consider, for instance, the qualitative difference, the difference in what it feels like or what it is like for one, between stepping on a nail and having a stomachache. What distinct pains are like for me to have seems—to me, from ‘the inside’—to vary considerably. They seem to me to be qualitative, to be like something for me when I introspect them, but their qualities vary. Consider for yourself: upon introspecting, do you find a distinctive pain quality? It is notoriously difficult to settle disagreements about qualitative character, but one thing which can help is to do our best to ensure that we are talking about the same thing. In particular, we should be careful to distinguish the supposedly distinctive pain quality, posited by the philosophical orthodoxy, from other qualities. In this section, we’ll carefully distinguish the posited pain quality from these other qualities, after which I will invite you to again consider the qualitative character of your pains. Consider first the sensory qualities of pain as reported. The McGill Pain Questionnaire (MPQ) is currently the most widely used and respected tool for reporting pain, and its qualities, for diagnostic purposes.5 In addition to offering descriptors for three non-sensory aspects of pain, it identifies ten major groups of common descriptors for the sensory aspect alone: Group 1: Flickering, Quivering, Pulsing, Throbbing, Beating, Pounding. Group 2: Jumping, Flashing, Shooting. Group 3: Pricking, Boring, Drilling, Stabbing, Lancinating.

34  The Need for Complexity Group 4: Sharp, Cutting, Lacerating. Group 5: Pinching, Pressing, Gnawing, Cramping, Crushing. Group 6: Tugging, Pulling, Wrenching. Group 7: Hot, Burning, Scalding, Searing. Group 8: Tingling, Itchy, Smarting, Stinging. Group 9: Dull, Sore, Hurting, Aching, Heavy. Group 10: Tender, Taut, Rasping, Splitting. None of these qualities are good candidates for the pain quality for the obvious reason that whichever we choose, some pains occur which lack that quality. Or, at least, some pains are reported as occurring and lacking that quality. Indeed, even particular pains can apparently vary in respect of these qualities over time, e.g. the pain in my stomach was aching and heavy and is now jumping and shooting. This suggests that these qualities are insufficient even for individuating one pain from another. None of the qualities identified by the MPQ can be the supposedly distinctive pain quality—none of these characterise the qualitative character supposed to be common to all (and only) pains. Of course, it may be properly objected that the pain quality is a much broader, more rough-grained, quality than any of the sensory qualities described in the MPQ. The obvious qualitative variation across token pains—i.e. distinct, individual, particular pains—or a single token pain across time undermines the idea that any such fine-grained qualities are common to all pains, but perhaps not that there is some more roughgrained quality common to them all. Perhaps all of the sensory descriptors above are just more specific ways the pain quality can be—even as crimson is a more specific way that something can be red, and red is a more specific way that something can be coloured. Red is a more finegrained quality than crimson, and coloured is more rough-grained than red. The pain quality may be a more rough-grained quality with more fine-grained qualities like burning, being a more specific way that quality can be. Even if so, the fine-grained sensory qualities reported using the MPQ are not the rough-grained distinctive pain quality which we are after. Accordingly, consider now the affective qualities of pain as reported. We report our pains as having not only sensory qualities, like those above, but as having affective quality—that is, as having an unpleasant quality. One might initially think that the distinctive pain quality just is the unpleasant way the pain feels. According to our everyday theory, pains do, after all, hurt. (At least, usually.) The unpleasant, nasty, ‘this stinks’ quality that is (at least) a paradigmatic feature of pain experiences according to our everyday theory may perhaps be thought to be the best candidate for the qualitative character in virtue of which a mental episode is pain. Despite their qualitative differences, all the mental episodes

The Need for Complexity  35 reported by employing the fine-grained sensory descriptors above may all be qualitatively unpleasant. The sharp pain of stepping on a nail and the dull pain of a stomachache, for instance, may both be unpleasant despite having different sensory qualities. Perhaps unpleasantness is the quality in virtue of which any mental episode is a pain. On this reading, the orthodoxy is challenged if we can image or identify any pains without unpleasant affect. Whether there are any pains which are not unpleasant was identified in the previous chapter as a question about which our everyday theory alone was not decisive; it is a question about which we might expect some of the people with whom we interact in our everyday lives to disagree. There are, however, good reasons to think that there are such cases. The intuition that pains are necessarily unpleasant may be deeply embedded for some, however (even if it’s not deeply embedded in everyday theory), so it is worth considering at least a few of these cases, dismissing alternative interpretations, and then to diagnose—and thereby hopefully explain away—the intuition. One class of examples of pains which apparently lack unpleasant affect are the chronic pains experienced by lobotomised patients.6 As Nikola Grahek (2011) points out (p. 31): The postoperative condition of patients who have undergone prefrontal lobotomies to treat chronic pain is often regarded as the paradigm case of an extreme reactive dissociation syndrome—or at least of striking indifference to pain. After the operation, these patients typically report that their pain is still present, but that it doesn’t bother them anymore, and/or that they do not mind or care about it anymore. Consider, similarly, the following case study of a lobotomised patient presented by Brand and Yancey (1997, pp. 210–211): By all measures, the lobotomy was a great success. The woman emerged from surgery completely free of the suffering that had shadowed her for a decade.… The husband spoke enthusiastically about the lobotomy, and the woman herself seemed calm and content. When I inquired about the pain, she said, “Oh yes, it’s still there. I just don’t worry about it anymore.” She smiled sweetly and chuckled to herself. “In fact, it’s still agonizing. But I don’t mind.” At the time it startled me … As I read about other lobotomies, however, I found she was displaying a very typical attitude. … Lobotomized patients rarely ask for medication. As a German neurosurgeon who had performed many frontal lobotomies once told me, “The procedure takes all the suffering out of pain”.

36  The Need for Complexity Freeman and Watts (1950) likewise present a number of case studies describing the experiences of lobotomised patients. Consider the following excerpt (p. 358): Pain in back since girlhood, worse since birth of first child 28 years ago, and unbearable for last three years. … Prefrontal lobotomy of the standard type… She says the pain is still there, but it does not bother her. It is important to note that only some pains experienced by lobotomised patients are not unpleasant; while pre-existing chronic pains are often no longer unpleasant, acute pains often still are.7 This suggests, however, that the difference for these patients is not in the way they report their pains, but is indeed a difference in the affective quality of the pains they are reporting. Though I think the lobotomised patients’ chronic pains are most naturally interpreted as lacking unpleasant affect, it is admittedly not the only interpretive option. At least two others should be considered. First, one might instead say that the pains of lobotomised patients are unpleasant, but that the patients are simply untroubled or unconcerned by the unpleasantness. The pain is unpleasant, one might say, but the patient doesn’t suffer from its unpleasantness. While the emotional response to pain’s affect may also change, this interpretation does not do justice to the seemingly very different post-surgical qualitative character of the pain itself, at least as reported. Both reports and behaviour indicate that the chronic pains are not unpleasant, while both also indicate that their other pains remain (at least, typically) unpleasant. The change, again it seems, is in the affective quality of the pain itself—that quality which we are currently considering may be the supposed pain quality. Second, one may say that the unpleasant affect of the chronic pains of the lobotomised is still always present, but that it is merely diminished or not consciously experienced. There seems, however, no independent reason to accept this interpretation; it explains nothing and is apparently inconsistent with first-person reports, behaviour, and useful diagnostic practice. It is an interpretive option that seems motivated solely by the desire to maintain the claim that pains are always unpleasant. For those not fully satisfied by these considerations, however, we briefly turn to pain asymbolics. The history of the term ‘pain asymbolia’ leaves plenty of room for disagreement about its extension.8 There are multiple pain dissociation syndromes—conditions in which some of pains’ paradigmatic dimensions are apparently present without others—and the terms used to refer to these syndromes have not always been employed systematically. However loosely we define the condition, however, there is a subset of pain asymbolics that seem to me to be accurately described

The Need for Complexity  37 as experiencing pains that are not unpleasant. Though particular theorists will undoubtedly disagree, I take this to now enjoy wide consensus not only across the philosophy of pain, but across pain science. Consider here a few classic cases.9 Berthier et al. (1988) describe their patients as reporting pain experiences that were not unpleasant (43, italics added): Although all 6 patients could adequately recognize painful stimuli and distinguish sharp from dull, all of them showed a lack of response to painful stimuli applied over the entire body. Neither superficial nor deep pain stimulation elicited a motor withdrawal, grimacing, or an appropriate emotional response … Inappropriate emotional responses were common: 4 patients smiled or laughed during the pain testing procedure. … while all could recognize pain, none of them reported any unpleasant feeling. Patients showed normal autonomic reactions (tachycardia, hypertension, sweating, mydriasis) during the painful stimulation, but failed to react with a flinch, blink, or adequate emotional responses…. Consider also the colourful case of a teenage boy presented by Frances and Gale (1975, p. 110): During pubescence he participated in sports and motorcycling with fearless abandon and an exhibitionistic flair. He began to demonstrate his ‘freakish’ but impressive insensitivity to pain by applying lighted cigarettes to various extremities. This often became a contest with other boys for both money and pride, with the patient the undefeated champion. …In spite of his clear cognitive understanding of his vulnerability to injury and the experience of numerous broken limbs, the patient participated without restraint in contact sports and frequent fist fights. …The patient describes his injuries with an indifference which would seem to belie the fact that they had happened to him. Paradoxically, he would be more upset by damage to his clothing than by bodily injury. Unfortunately, these latter authors conflate what pain researchers now distinguish: pain insensitivity and pain indifference. Pain insensitivity is a condition whereby individuals do not report any pain and cannot reliably discriminate among various noxious stimulations. Pain indifference, by contrast, is a condition whereby individuals can reliably discriminate among noxious stimuli and do report experiencing pain, but are indifferent to the experience. The case in question is of an individual who reported pain, and knew he was being injured, but was not bothered by either his pain or his injuries. He would now be properly diagnosed with pain indifference, not pain insensitivity: he reports feeling

38  The Need for Complexity pain, but the pain he feels is not reported as being unpleasant, nor does he behave as if it is. Confronted with these cases of pain asymbolia, retaining the claim that pain always has unpleasant affect requires embracing one of two interpretive options: either these individuals are wrong that what they are experiencing is pain, or they are wrong about whether the pain that they are experiencing is unpleasant. Both options should be rejected. The second option is the weakest. The lack of withdrawal response or aversive reaction one would predict of an unpleasant experience tells against declaring that the subjects have systematically inaccurate reports. Indeed, independent of the intuition in question, it is hard to see any reason for construing these subjects as undergoing unpleasant mental episodes. The lack of not only verbal, but non-verbal behaviour indicating unpleasant sensations tells against positing non-conscious or diminished unpleasant affect. If their identification of these experiences as pain is based on its qualities at all, it is apparently not on the basis of its unpleasant affective quality. The first option—denying that what the subjects are experiencing is pain at all—may be more tempting. Consider this final heart-rending case described by Osuntokun et al. (1968, pp. 291–292, emphasis added): … a 5-year-old boy … rarely cried, but shed tears normally when he did and appeared incapable of being easily hurt … There was no history of excessive or diminished sweating [a typical symptom of pain insensitivity as against pain indifference] … Neurological examination showed normal sensorium. … There was no detectable abnormality in the motor system, the muscles, the gait, and coordination being normal. In the sensory system light touch was normal. … His reaction to noxious stimuli was, however, odd. … He showed no withdrawal response, evasive or preventive motor reactions, and no facial expression of pain to pin-prick venipuncture, intense pressure on the Achilles tendon, or to his skin being transfixed with a needle—which he seemed to enjoy very much. He invited the examiner to repeat the tests while he remained all smiles. … The patient was in hospital for eight weeks, during which news got around of the ‘wonder boy’ who could not feel pain. Subsequently … some laboratory technicians surreptitiously paid him several visits, transfixing him with pins and needles and watching with awe how much he enjoyed it. He appeared, however, to discover that he was being regarded as a ‘freak’ and developed the greatest dislike of pins and needles. This child’s ability to discriminate among noxious stimulation (intensity, burning/pricking/stinging, etc.) and the well-functioning of his

The Need for Complexity  39 autonomic and motor systems allowed the doctors to diagnose him with pain indifference and not pain insensitivity. Notice, however, that in the face of this boy’s pains which were not unpleasant, rumours spread that he could not feel pain at all. Given that our everyday theory does not alone decisively settle whether mental episodes reported as pains that are not unpleasant are really pains, this is unsurprising. Two major theoretical considerations point against interpreting pain asymbolics like this child as not experiencing pain. First, the individuals report their mental episodes as pains. First-person reports—our reports about our mental episodes ‘from the inside’—should be accepted as accurate unless there is good reason to reject them. Whether the bare intuition that pains simply must be unpleasant is sufficient to reject first-person reports is arguable and, in the present context, questionbegging, i.e. it assumes what’s at issue. Second, and more important, are these asymbolics’ abilities to discriminate the intensity and other qualities of their pains. Again: people with pain insensitivity neither reliably distinguish among noxious stimulations, nor report any of their experiences as pains. People with pain indifference like this child, however, both reliably distinguish among noxious stimulations and report some of their experiences as pains. Insisting that what they are experiencing is not really pain appears to be arbitrary linguistic legislation. It’s not required by our everyday theory, it’s inconsistent with their reports, and it’s unhelpful for any diagnostic purposes. Though our everyday theory does not commit us to the idea that pains must be unpleasant and the clinical evidence suggests that they are not, why might some nonetheless have the strong intuition that pains are always—even necessarily or essentially—unpleasant? I suggest this has happened because the unpleasant affect we paradigmatically experience when in pain is often its most important feature; unpleasant affect is often the central reasons that we care about our pains, and that we are motivated to do something to rid ourselves and others of them. Those who hold that pain is always, necessarily, or essentially unpleasant thus seem to me to have made an understandable mistake: they have confused the importance of this feature with some other feature, e.g. necessity or essence. Note that the mistake of confusing importance with essence is one that Kripke himself (1980, p. 77) warns against: “Important properties of an object need not be essential … an object could have had properties very different from its most striking actual properties, or from the properties we use to identify it”. Applied to pain: the importance of pain’s unpleasant affect may lead one to infer that it is essential. As Kripke himself argues, this inference is illegitimate. The same considerations hold for the weaker claim that pains are necessarily, or always, unpleasant. The temptation to think of unpleasantness as necessary or essential to pain, despite actual cases of pains that are not unpleasant, is neatly explained, and plausibly explained

40  The Need for Complexity away, by pointing out that this confuses what is important about many pains, with what must always, necessarily, or essentially be true of them. The importance of affect may make this intuition very strong for some, but actual cases of pains that are not unpleasant warrant abandoning it. Recall that we are currently considering an interpretation of the orthodoxy of simplicity, according to which the pain quality—that supposed quality in virtue of which a mental episode is a pain—is unpleasant affect. This interpretation of the orthodoxy is challenged not only by pains which are not unpleasant, but by mental episodes with unpleasant affect which are not pains. And while pain asymbolia, lobotomy, or similar cases that supposedly evidence pains which are not unpleasant may be surprising and somewhat controversial, a profundity of cases of unpleasant mental episodes which are nonetheless not pains are humdrum. Such cases abound. Many mental episodes have unpleasant affect, but are nevertheless not pains. As we noted in the previous chapter, our everyday theory will not by itself settle whether any emotional episodes are really pains. The so-called ‘social pains’ of rejection, grief, jealousy, and heartbreak, for instance, have recently been posited by some social psychologists and neuroscientists as constituting a distinct class of pains. While specialised theorising may appropriately be employed here to help us determine whether these emotional experiences should be classed as pains,10 a yet wider range of unpleasant mental episodes more obviously fail to be pains. Consider nausea, annoyance, disgust, dizziness, boredom, or tiredness. While a powerful theory may convince us to revise our everyday theory and accept instandes of these paradigmatially unpleasant mental episodes as pains, a powerful theory would here be needed. In everyday life: when I have the disgusting experience of smelling rotten meat, the annoying experience of hearing the music of Phillip Glass, or the boring experience of sitting in yet another committee meeting, I neither class nor report these unpleasant experiences as pains. Or, if I do report these experiences using pain language, I do so merely metaphorically. These are not, as we might say in everyday life, really pains. They are, however, mental episodes with unpleasant affect. They are really unpleasant. Unpleasant affect and pain are thus distinct and doubly dissociable— facts which are now widely accepted in the science of pain and affect, as well as by most dominant, contemporary, analytic philosophers of pain. While the existence of pain without unpleasant affect may be controversial from the point of view of everyday theory, evidence from the clinic suggests that such pains are not only possible, but actual. Going further, mental episodes with unpleasant affect that are not pain are blithely reported and accepted in our everyday interactions. If there is a distinctive pain quality, unpleasant affect is not it. We should not here

The Need for Complexity  41 overcommit everyday theory and hold that pains are all and only those mental episodes with unpleasant affect. If the above considerations are correct, neither the sensory nor affective qualities of the mental episodes we report as pain are the supposedly distinctive, qualitative character posited by philosophers. That is, the sensory and affective qualities of pain are not the supposed pain quality which all and only pains are held by the orthodoxy to have.11 In light of this, recall INTROSPECTION: INTROSPECTION: Whenever I introspect my pain experiences, I find a distinctive, qualitative character—a ‘what it is like for me’—that is common to them all. We can now see clearly that we might deny INTROSPECTION and still accept that pains paradigmatically have qualitative character; in particular, one might think that the qualities of pain, found upon introspecting, are combinations of sensory and affective qualities. One may even hold that these qualities—or even some particular combinations of them—are necessary, sufficient, or essential to pain, and still deny INTROSPECTION. INTROSPECTION requires not only that pains are like something for you to have, but that what they are like for you to have is something distinct from any of the sensory or affective qualities discussed above. I encourage those who take INTROSPECTION to be true of their own introspection to carefully consider whether it is indeed truly the pain quality which they find to be common across all their pains; or if, instead, they find combinations of sensory and affective qualities, none of which is a distinctive pain quality. Does the experience of an unpleasant, burning pain in your finger have—in addition to the unpleasant affect and the burning sensation—a distinctive pain quality? Does the experience of an unpleasant, wrenching pain in your stomach have—in addition to the unpleasant affect and wrenching sensation—a distinctive pain quality? Again, I simply report my own introspection when I deny finding any such distinctive quality. Note that disagreement about whether introspection facilitates access to the posited pain quality may itself pose a problem for reconciling the orthodoxy of simplicity with some views of qualitative character. We might, that is, disgaree about just how much considering episodes ‘from the inside’ can tell us about the qualities of those episodes, or whether there is any other way we might learn about those qualities. One might hold, as Kripke himself seems to hold, that the only access to our mental qualities which we have is first-personal—i.e. from ‘the inside’. If so, however, then it seems that the only theoretical tool that we can use to evaluate the orthodoxy of simplicity are those pain reports which

42  The Need for Complexity are expressions of first-personal access. If we accept this view, however, then it would seem that we fail to vindicate the orthodoxy: a distinctive pain quality is reported by some, perhaps, but not others. If the only access we have to qualitative characters is simply as being whatever they are reported to be, then there is a distinctive pain quality for some pain experiences and not others—since that’s what’s reported. Accordingly, if we accept this brute, first-personal theory of qualitative character, then we should reject the orthodoxy of simplicity, which claims that pains are all and only those mental episodes with the pain quality. Notice that the argument in the previous paragraph reverses the standard order of philosophical theorising about pain. On the standard line of thought: pains are supposed to be all and only those mental episodes with the pain quality, and an account of qualitative character is evaluated for its adequacy in accounting for that supposed quality. In the previous paragraph: a theory of the qualitative character of the supposed pain quality is granted, and is argued to fail to yield an adequate account of pain. Though the simplistic view of the pain quality presented in Kripke does not currently dominate philosophical theorising about pain, I will deploy a similar strategy to argue against those accounts of the pain quality which do. Drawing on pain reports from everyday life and clinical observations, in the next two sections I argue against the leading, intentionalist, theories of pain. In particular, I argue that accounts of the pain quality as explained by a distinctive, representational content (Section 2.3) and as explained by a distinctive, imperatival content (Section 2.4) are inadequate. As an argument against the orthodoxy of simplicity, this strategy is obviously limited: though simple qualitative accounts (as above) and intentionalist accounts of the pain quality (Sections 2.3–2.4) dominate and (I argue) fail, perhaps we simply need a better theory of the posited pain quality. I consider (Section 2.5) the prospects of a psychofunctionalist account of the pain quality, which rejects a distinctive content for the pain quality and appeals directly to pain science. Through this discussion we will begin to directly consider the status of the supposedly distinctive pain quality in life, science, and medicine, and turn directly to pain science in the following chapter.

2.3 The Pain Quality Explained by a Distinctive Representational Content It’s a platitude of our everyday theory that many of our mental episodes are about something: my belief that my coffee is hot and my desire to drink my hot coffee are both about my coffee. We regularly report, and ask each other, what our thoughts, regrets, wishes, and plans are about. Call this about-ness intentionality. And notice that it’s not only mental episodes which our everyday theory accepts to have intentionality:

The Need for Complexity  43 speech, sentences, gestures, symbols, or images can all, we typically think, have intentionality, i.e. they can all be about things. Stories, as a paradigm example, have intentionality; stories are about something. In everyday life, we might refer to what a story is about as the content of the story. So too, many theorists working on intentionality refer to what a mental episode is about as the content of the mental state. The intentional content of my belief is that my coffee is hot—my coffee being hot is what my belief is about. The intentional content of my desire is that I drink my hot coffee—my drinking the hot coffee is what my desire is about. As one might expect, there are different theories about intentionality, i.e. about the way in which mental episodes—or any other candidate intentional entity—get to be about things. Representation is one form of intentionality; one way for something to be about something else is by representing it. Stories in a newspaper, as in the above example, apparently have this form of intentionality: the language which constitutes the story represents the events which the story is thereby about. Many philosophers hold that mental episodes like beliefs and desires also have this same kind of representational intentionality. Beliefs and desires seem to be about the world in virtue of representing it. Even as the newspaper story might represent that Germany is out of the World Cup, so my belief represents that my coffee is hot and my desire represents that I drink the hot coffee. While the newspaper story uses language to represent the world, there isn’t yet agreement about how our mental episodes do it: whether we use a mental language, mental imagery, a combination of these, or something else entirely. Note finally that our attitudes towards representational contents differ. I can, for instance, either believe or desire that the world be a certain way. Beliefs and desires are different mental attitudes that I can have. The differences between these mental attitudes are enshrined in how we evaluate them in our everyday life: my belief that my coffee is hot is evaluated as true if my coffee is hot (and false, if it isn’t), whereas my desire that I drink my hot coffee is evaluated as satisfied if I drink the hot coffee (and frustrated, if I don’t). Beliefs, however, aren’t satisfied or unsatisfied, and desires aren’t true or false. But both attitudes represent the world to be a certain way and both involve representations which we can evaluate. In one case, I represent the way that I believe the world to be and the representation can be true or false, and in the other case, I represent the way that I desire the world to be and the representation can be satisfied or unsatisfied. According to representationalist theories of the mind (RTM), as forcefully pioneered in analytic philosophy by David Armstrong (1962a), all mental episodes are representations. (However, exactly, they manage to represent.) This includes not only mental episodes like beliefs and desires, as mentioned above, but also mental episodes with qualitative character like perceptions and sensations. On a representationalist view,

44  The Need for Complexity qualitative character is to be explained by representation—either what is represented or how it’s represented. What explains the colour qualities of my visual perceptions—the redness, blueness, and so on, of my visual perceptions—is either what in the world those perceptions represent or how they represent it. On the strongest versions of representationalism, qualitative character is not only explained by its representational features but depends, or even consists, on those representational features. On these views, the blue quality of your seeing the blue sky, what it’s like for you to have that blue visual experience, depends, or even just is, your representing the blue of the sky.12 Since representations seem to be a ‘non-spooky’ phenomenon which we can scientifically study, a central motivation for RTM was that it has seemed to many to promise a way to naturalise the mind, i.e. to explain the mind and all its features in a scientifically respectable way. As RTM rose to prominence, pain was quickly identified as a challenge. It seems undeniable that pains, at least typically, have qualitative character; it is typically like something for one to have a pain experience. As per the orthodoxy, pains were accepted to be just those episodes with a distinctive qualitative character. Along with other bodily sensations like tickles, itches, and orgasms, however, many found it hard to accept that the qualities of these sensations could be explained by their representational features. Representational episodes represent the world to be a certain way, but pains seemed to some not to do this. Colin McGinn (1982, p. 8) puts the classic worry this way: We distinguish between a visual experience and what it is an experience of; but we do not make this distinction in respect of pains. Or again, visual experiences represent the world as being a certain way, but pains have no such representational content. One way to see the force of the challenge is to consider that if pains represent the world, then it should be possible for them to represent the world as being a way that it is not—that is, for them to misrepresent the world. Think again about content. If we take the qualitative character of pain to be explained by its representational content, then pain should have a content which represents that the world is a certain way. And it seems that it then should be possible that the pain’s content, just like the contents of a story in a newspaper, could be inaccurate. The news could be ‘fake news’. If pains are representational, a pain could be a ‘fake pain’. But, some think, this simply is not possible when it comes to pains. Unlike other things which represent the world to be a certain way, pains aren’t accurate or inaccurate, much less true or false. There are no pain hallucinations or illusions in the way that there are visual hallucinations or illusions. A pain can’t be false in the way a newspaper story could be.

The Need for Complexity  45 If pains are all and only those mental episodes with the pain quality, but pains do not represent, then representationalism for qualitative character fails. The challenge for the philosopher who wants to accept RTM and the orthodoxy of simplicity is then to identify what pains represent. What are pains representations of? What in the world are pains about? Armstrong himself (1962b) rose to this challenge, arguing that pains are bodily sensations which represent bodily disturbances at, or in, bodily locations. Bodily sensations are held to be especially indistinct, so we may be imprecise about both the nature of the disturbance and its precise location, i.e. we might be uncertain about exactly where the pain is or exactly what kind of pain it is. To be a pain, however, is to be a mental state which represents located bodily disturbance of some kind, in some place. The theory is intended to defend the representationalist account of qualitative character in general, by offering an adequate account of pain in particular—an account which is taken to be required because the orthodoxy of simplicity, which posits that there is a distinctive pain quality, is accepted. Notice that the account specifies when a pain is accurate or inaccurate. As pains are those mental episodes which represent located bodily disturbances, if there is no such located bodily disturbance, then the pain is misrepresenting the world. If there is no bodily disturbance at all, then the pain (which represents that there is) will be hallucinatory. If there is a bodily disturbance, but it is not how the pain represents it to be—it isn’t where it is represented to be or as it is represented to be—then the pain will be illusory. Note that a hallucinatory or illusory pain is a real pain, but it is also a real hallucination or illusion. On this account, some pains represent the world inaccurately, but they are still pains for all that. Notice that this account of pain is not supposed to explain the unpleasant affective quality that is paradigmatic of pain. According to Armstrong, the unpleasant affective quality that we often report our pains to have is to be explained by an ‘immediate dislike’ of the pain. The pain quality, in virtue of which the mental episode is a pain, is one thing, and the affective quality, in virtue of which the pain is unpleasant, is another.13 It’s worth stressing that Armstrong takes our everyday theory of pain to be more inclusive than the specialised representationalist theory of pain which he defends. According to Armstrong, our everyday notion of pain is a ‘portmanteau-concept’, encompassing both the representation of located bodily damage and unpleasant affect. Armstrong thus acknowledges that our everyday theory does not decisively settle whether cases of pains that are not unpleasant should be classed as pains or not, i.e. whether they are really pains. He writes that “… a linguistic decision has to be taken as to whether they [reporters of such pains] can be said to be feeling ‘pain’ or not” (p. 108). As above, he thinks the right decision is

46  The Need for Complexity to accept that these are really pains: a pain is a representation of located bodily disturbance, and unpleasant affect is a reaction to this representation. The unpleasantness of pain is to be explained by how we react to pain, but it is not a part of the pain itself. But by Armstrong’s own lights, this is not our everyday theory. Accepting Armstrong’s representationalism would instead involve revising our everyday concept. We will return to the idea that accepting dominant philosophical theories of pain requires revising our everyday concept in Section 2.5. Developments and disagreements in representationalism for pain have focussed on affect, retaining Armstrong’s account of the pain quality almost entirely unchanged. Evaluativism for unpleasant pain, in particular, is currently dominant.14 On this view, as per the orthodoxy, pains are all and only those mental episodes with a distinctive qualitative character, i.e. the pain quality. And as per Armstrong, the pain quality is to be explained by a representation of located bodily damage. Departing from Armstrong, however, a pain is unpleasant in virtue of an evaluation of the located bodily disturbance represented by the pain, e.g. as bad or harmful. Pains are unpleasant because they represent some disturbance in your body as being bad for you. On this contemporary view, then, unpleasant pains not only represent that there is located bodily disturbance, but crucially, they also represent that located bodily disturbance as bad. Contemporary focus on how representationalists might explain pains’ unpleasantness makes some sense; it is, in particular, evaluative content that is supposed to explain many of the normative and motivational features of unpleasant pain focussed upon in much recent philosophical work, i.e. how, when, and whether pain gives us good reasons to do things and motivates us to do things.15 The account of the pain quality as a representation of located bodily disturbance, however, has remained dominant and undeveloped in even contemporary, evaluative representationalist theories of unpleasant pain. So, Brian Cutter and Michael Tye (2011, 92) write: Consider your experience of a pain in a forearm. … the content of your experience is something like: there is a disturbance of type d in location l. (Here we should assume that the physiological type d includes information about the shape, volume, and intensity of the disturbance, e.g. whether it is mechanically, thermally, or chemically induced.) In brief, tissue damage or disturbance … is what pain experiences represent. Their discussion and defence focusses upon how the theory can be extended to explain unpleasant pains by adding further, evaluative, content, such that the mental episode is about not only bodily damage but how bad or harmful that damage is for the person suffering it. As is typical, little attention is paid to the non-evaluative content, i.e. the

The Need for Complexity  47 representation of the located bodily disturbance. Armstrong’s early account of the supposed pain quality is simply taken for granted. David Bain (2017, pp. 40–41) similarly defines evaluativism for unpleasant pain this way: 1 2

Your being in pain consists in your undergoing an interoceptive experience (the pain or pain experience) that represents a bodily condition of a certain sort. Your pain being unpleasant consists in its additionally representing that condition as bad for you.

He immediately goes on to say (p. 41): Notice the following. First, like most accounts of unpleasant pain, this is a composite view, invoking the distinct ingredients to explain pain and its unpleasantness respectively. This structure makes room for pains that are not unpleasant… Suppose your pain yesterday was unpleasant and your otherwise identical pain today isn’t (thanks to morphine, say). For evaluativists, this is a matter of the two pains representing the same kind of bodily condition, but only yesterday’s representing it as bad for you. The view of unpleasant pain is indeed composite and complex; but—as with the view pioneered by Armstrong—the view of pain remains consistent with the orthodoxy of simplicity. The definition of pain is given in condition 1, whereas the definition of pain’s unpleasantness is given in condition 2—and this second condition gives the view its name. For present purposes, however, we are interested in the theory of pain (condition 1 above, and as originally offered by Armstrong). We are not focussed on the theory of affect or unpleasantness: as per our everyday theory, many mental episodes which aren’t pains are sometimes unpleasant, and as per our best clinical evidence, at least some pains are not unpleasant. Armstrong, Cutter, Tye, and Bain all accept that pains are all and only those mental episodes with a distinctive qualitative character (i.e. the pain quality) and that this quality is to be explained by the representation of located bodily disturbance. On these views: as per the orthodoxy, what makes a mental episode a pain is its distinctive qualitative character, and what explains that distinctive qualitative character is that the mental episode represents a located bodily disturbance.16 What I will now argue is that this is inadequate as an account of pain— whatever the status of the posited evaluative account of unpleasantness. The problem, in short, is that the correlation between pain and bodily disturbance is poor. It’s not merely that there are a few mismatches, which we might accept. Instead, the lack of correlation is profound. Two broad types of cases are problematic. First, mental episodes which are

48  The Need for Complexity plausibly pain, but which aren’t plausibly inaccurate representations of located bodily disturbance, i.e. these episodes aren’t plausibly hallucinations and illusions. Second, mental episodes which aren’t plausibly pain, but which plausibly are accurate representations of located bodily damage. In short, accepting this representationalist account of pain would deem too many pains hallucinatory or illusory, and too many non-pains would be deemed pains. The correlation between pain and what they supposedly represent is too poor for us to accept the theory; it delivers the wrong verdict in too many cases. It’s not plausible that pains are all and only those mental states which represent our bodies as being disturbed in a certain place, in any certain way. For evaluating the theory, we need to be careful in specifying exactly what pains are supposed to represent. It’s clear that if we leave the type of bodily disturbance completely unspecified, then far too many pains will be deemed to be pain; if pains are the representations of any bodily disturbance, then tickles, itches, pressure, twitches, and many more will all be deemed pains by the theory. On the other hand, specifying the particular type of bodily disturbance will make the theory more vulnerable to hallucinations and illusions; any time we are in pain, but not undergoing the particular type of bodily disturbance specified, we’ll be suffering from a hallucination or illusion. Representationalists recognise the need to further specify the supposed type of bodily condition represented by pains. As quoted above, for instance, Tye and Cutter characterise pains as being about ‘a disturbance of type d’, and Bain uses the phrase ‘bodily conditions of a certain sort’. Not any old representation of located bodily disturbance will do. Not much effort, however, has gone into defending exactly what sort, or type, of bodily condition is represented. What is type d? What is the certain sort? Tissue damage is the most common candidate. Tye and Cutter themselves, for instance, mention it in the quote above, and it occurs frequently in the literature. We’ll briefly consider whether some other type of bodily condition may be a better candidate at the end of this section, but let’s begin by using this central one on offer. In challenging the adequacy of the theory, consider first the glut of pains which the account deems to be hallucinations and illusions: these include all pains which are not accurate representations of located tissue damage. Here is a brief and partial catalogue: II Lower-back pain: Another common problem, lower-back pain usually involves no damage to the lower back. Loeser and Volinn (1991) reports that there is no known tissue damage in 70% of these cases.

The Need for Complexity  49







These are all cases of pain without any tissue damage at the location where the pain is experienced as being. On the present account, they are all, therefore, either not pains at all, or cases of hallucination or illusion. While a plausible interpretation for some cases, it is less so for others. Are headaches, for instance, hallucinations? One reason to reject that these are all hallucinations and illusions is to flatly appeal to our intuitions about these cases. We ought not to posit more hallucinations and illusions than is necessary. While it is difficult to know when many hallucinations or illusions are too many, it seems to me that the cases above are far too many.17 I think we would need some very strong reasons to take all of the above as hallucinations or illusions, and I do not think that there is any such strong enough reason to accept that they are. Indeed, independent of the theory we are currently testing, it is hard to see any reason to think that, e.g., headaches are hallucinations.

50  The Need for Complexity While I find it implausible to characterise all of the above (and similar) cases as hallucinations or illusions, it is nonetheless certainly open to the representationalist to do so. And, unlike me, they may be quite sanguine about it. In particular, to attempt to render credible the seemingly implausible, representationalists may appeal to a particular theory of representational content. Theories of representational content aim to explain how and why representations have the content that they have. Perhaps such a theory could explain why pains are—according to the representationalist—always about located tissue damage, despite the fact that there so often fails to be any such damage when we are in pain. Teleological theories of intentional content, in particular, might seem to help. On these views, in brief and roughly, mental episodes have their contents in virtue of the way that they are produced or used, i.e. by their function. On these views, to tell a story about why a mental episode has the content it does, we identify what that mental episode is for. What, we ask, is its function? A teleological representationalist may answer that the function of pains is to inform us about damage to our bodies’ tissues and that located tissue damage is, therefore, what pains represent. Informing us about damage to our bodies’ tissues is what pains are for. If we think about this function and this content, from an evolutionary perspective, the glut of misrepresentations may begin to appear acceptable. We might think that it’s more evolutionarily advantageous to represent our bodies as damaged in many cases when they aren’t, then to fail to represent our bodies as damaged when they are. It may be best, from an evolutionary perspective, that we have a glut of ‘false positives’ for located bodily damage. Having so many misrepresentations may help pains better fulfil their evolutionary function. The predictions of any such theory of representational content, however, fail for pain. All theories of representational content commit to some systematic link between the mental episodes and what they represent. Many of these stories are intended to be scientifically respectable, ‘naturalist’, stories—indeed, this is supposed to be a central attraction of RTM. But the correlations that adopting any of these naturalistic theories of content would predict are lacking. Cutter and Tye (2011), for instance, explicitly advocate a kind of (teleological) tracking theory of representational content for pain. The details here get technical and most don’t concern us. Notice merely that the view is committed to a distinctive system, selected for through natural selection, which produces pains—taken to be a distinctive representation with a distinctive function. The best candidate for a system which produces representations of tissue damage is the so-called nociceptive system. ‘Nociceptor’, however, is largely a heuristic for receptors which

The Need for Complexity  51 preferentially respond to noxious stimulation (Craig, 2003). No type of receptor is unresponsive to noxious stimulation, and those which are preferentially responsive to it are nonetheless often responsive to non-noxious stimulation. The result is that so-called nociceptors are a loose subset of receptors that, in fact and in general, respond to all manner of thermal, mechanical, and chemical stimulation. Activity in these receptors, and the processing of this activity, results in all sorts of bodily sensations—many of which are non-controversially touch and not pain. So too, pains frequently occur without any activity whatsoever in these receptors. Accordingly, even if nociceptors are granted as a robustly distinct processing system, activity in this system doubly dissociates from pain. Indeed, as we’ll consider in more detail in the next chapter, pain scientists now clearly distinguish between pain and nociception—on the very grounds that pain is poorly correlated with the workings of this system. The moral is that the very existence of a system which tracks and informs us about tissue damage is somewhat controversial, but it is uncontroversial that pain should be neatly distinguished from activity in any such system so-far identified, i.e. from nociception. Indeed, I’ll ague directly in the next chapter that there is no such system. While appealing to a naturalistic theory of representational content may have helped deal with the glut of cases the theory would deem hallucinations and illusions, the empirical support needed to make good on such an appeal is apparently lacking. Finally, remember that a specialised theory of pain should be useful for explanation and prediction, and that the most important purpose for testing explanatory and predictive success is treatment. I now submit that adequate treatment requires that we avoid relegating so many pains to the realm of hallucinations and illusions. As Melzack and Wall (1998) pointed out when introducing their revolutionary model of pain 50 years ago: a model of pain needs to be adequate for use by clinicians when called upon to respond to pain in the clinic—and this explicitly includes the great many pains which are reported in the absence of any tissue damage. From a practical perspective, classing this wide range of cases as hallucination or illusions is preposterous. Dismissing cases of fibromyalgia, for instance, as if they are some kind of misrepresentation, has had disastrous therapeutic consequences.18 We must remember: it is treatment above all that we want our specialised theories of pain to be explanatory and predictively useful for. I take the un-intuitiveness, lack of empirical support, and therapeutic implications to be strong reasons against classing all of the many cases of pains reported in the absence of corresponding located tissue damage as hallucinations and illusions. Consider now the second class of problematic cases for our representationalist: mental episodes which aren’t plausibly pain, but which

52  The Need for Complexity plausibly are accurate representations of located tissue damage. Here is a brief catalogue of some such cases:











The Need for Complexity  53 These dissociations between the representation of tissue damage and pain further undermine the plausibility of the representationalist account. Insofar as all of the above cases involve the representation of located tissue damage, the theory deems them all pain. This is implausible. What might the representationalist say about these cases?19 Notice first that it apparently won’t do to say that the representations of tissue damage are of the wrong kind. Recall that condition 1, presented in Bain (2017 and as above), specifies that pains are interoceptive representations. ‘Interoception’ is a broad label for the processes whereby one perceives the internal states of one’s body. This is to be contrasted with exteroception, through which one perceives things external to the body. Vision and hearing, for instance, are types of exteroception: they allow us to perceive things outside of our bodies. If we do not add the interoceptive qualification to the representationalist account, then there will be many more problematic cases than those listed above; without this qualification, seeing that my tissues are damaged in a certain bodily location, for instance, would be deemed pain by the theory. We’ve not yet mentioned this further complexity for the representationalist account, but let’s now grant that they can deal with it by appeal to interoception or something similar. 20 It may be tempting to try to deal with the above cases by claiming that the representations aren’t generated by the right kind of system, such that even though these are representations of located tissue damage, they are generated by the wrong system, and so lack the pain quality—and, consistent with the orthodoxy, that’s why they aren’t pains. All of the above cases, however, are apparently (and apparently accurate) cases of interoceptive representations of tissue damage, if any cases of pain are; they seem to be generated in the same sort of way as other representations of tissue damage taken by the representationalists to explain pains. It’s not a difference in which system generates the representations, then, which might explain why they nonetheless fail to be pain. What else might the representationalist say? Most obviously, they could say that all of these people are in pain, despite, when asked, their protestations to the contrary. Perhaps all of these subjects are either pretending not to be in pain, unaware of their pain, or are just plain wrong about whether they are in pain. For some reason or other, perhaps all such subjects are really in pain, despite their reports that they are not. I find this incredible. Notice that the problem is not just that the experiences of these subjects are not unpleasant; we should accept that affect and pain doubly dissociate. The problem is that there is no reason, besides the accurate report of tissue damage itself, to accept that these people are in pain. Notice, for instance, that excepting the congenitally insensitive to pain, these people’s general capacity to accurately identify

54  The Need for Complexity their other pains as pain is intact: people in the above cases report all of their other pains without difficulty, and those reports are unproblematically accepted. The boxer who can accurately describe the damage to his tissues when arriving at the hospital, and denies feeling pain until hours later, is not considered mistaken in any of their other reports, expressions, or descriptions of their pain. And why should they be? Indeed, many of us are likely to have experienced multiple bouts of episodic analgesia. It seems incredible that in all such cases, even when attending to our experiences, we are mistaken or unaware of our pains. It would, I submit, be absurd to tell the trepanation patient that they are in pain and simply fail to realise it. It would be absurd to tell the person engaging in SIB that what they are feeling is not relief, but pain of which they are unaware. Not only do I think that any such move by the representationalist would be incredible, but notice again that the implications for treatment of deeming all such cases pain—pains about which the subjects are unaware or somehow mistaken—again tells against the representationalist account. As noted in the previous chapter, the poor correlation between pain and injury has led the IASP to adopt a purely subjective criteria for pain; pains are so poorly correlated with injury that we are advised to take only the report as criterial for treatment purposes. As discussed further in Chapter 4, while I think that we should instead leave open the possibility that we are sometimes in pain even when we deny it, and sometimes not in pain even when we report it, it would nonetheless be therapeutically problematic to consider all instances of the above kinds of cases in this way. It would, for instance, be disastrous for emergency service clinicians to take all those patients arriving with (represented) injuries as being in pain, despite their denials. It would be problematic, for the purposes of treatment, to insist, against their reports, that those engaging in SIB are all in pain—whatever they think—whenever they damage their tissues and (even interoceptively) represent that damage. And, yet again: it is treatment above all for which our specialised theories of pain should be useful. Recall the challenge of pain for the representationalist: if pains are all and only those mental episodes with the pain quality, but pains do not represent, then representationalism for qualitative character fails. Since Armstrong, representationalists have responded to this challenge by holding that pains represent located bodily disturbances and, sometimes more specifically, tissue damage. I’ve argued that pains, as reported in everyday life and requiring treatment in the clinic, are too poorly correlated with tissue damage for this response to be adequate. Tissue damage isn’t what all and only pains are about. One obvious way that a representationalist might respond is by altering the claim about what pains represent, i.e. to fiddle with the posited representational content.21 They may save the theory by identifying

The Need for Complexity  55 something else that all and only pains are more plausibly about. Perhaps, for instance, pains do not represent tissue damage, but some other type of bodily disturbance. But what type? The answer is far from obvious. Remember, it cannot be that pains are all and only those mental states which are about any bodily disturbances whatsoever—too many representations of bodily disturbances are patently not pains, e.g. tickles, itches, orgasms, and more. There is, to my knowledge, no available candidates more scientifically or clinically respectable than tissue damage. And this candidate fails. In hopes of identifying an alternative representational content, a representationalist may look to pain science. While the appeal to a biological system which produces representations of tissue damage (i.e. nociception) failed, perhaps the representations produced by some other system will prove more successful. In particular: if there were a pain mechanism or system, with the function of producing representations, then the representationalist may try to appeal to the functioning of that system and its representations. The biological system for tactition won’t work, and neither will the so-called nociceptive system, but perhaps there is another which will. We may, that is, be able to hold that pains are all and only those representations, produced by a distinctive pain system. Whatever the representations of the pain system are about, that’s what pains represent. I’ll argue directly in the following chapter that there is no such system. For now, however, notice that an alternative response is open to the representationalist: they can reject the orthodoxy of simplicity. In defending their theory of qualitative character, representationalists responded to the challenge of pain by offering an account of what the pain quality represents. But they may, instead, simply deny that pains are all and only those mental episodes with a distinctive qualitative character. I urge the committed representationalist to consider this alternative. In recent years, however, another alternative which may maintain both the orthodoxy of simplicity and the claim that all qualitative character is explained by (or stronger: depends on or consists in) intentional content has been offered. On this alternative view, pains are about the body, but rather than representing it, they command the pained to take action concerning it. We turn now to this alternative.

2.4 The Pain Quality Explained by a Distinctive Imperative Content Representation is one way that something can be about something else, but there are others. Stories in a newspaper, recall, have representational intentionality; the language which constitutes the story represents the events which the story is thereby about. But language, in particular, is apparently sometimes used not only to represent things, but to express

56  The Need for Complexity our attitudes towards them. We don’t, that is, exclusively use language to make assertions: we question, muse, request, interrogate, and more. When I ask if you are thirsty, my question is about you (and your levels of thirst), even though my question doesn’t represent you as being a certain way—indeed, the purpose of my question is to find out whether you are a certain way. My question has intentional content, but not representational content. Linguists classify some of the different ways that we use language to express our attitudes about things grammatical moods. For our purposes, we need only distinguish between what’s called the indicative mood and the imperative mood. Our language is characterised as being in the indicative mood when used to express what we think is the case, i.e. when we use it to indicate. When I say, ‘The coffee is hot’, the sentence I use is likely in the indicative mood—I am likely using it to express what I think is the case. By contrast, our language is characterised as being in the imperative mood when used to express a request or command, i.e. when we use it to issue imperatives. When I say, ‘Bring me that coffee’, the sentence I use is likely in the imperative mood—I use it to request, or command, that something be done. A central reason that it’s useful to distinguish these different grammatical moods is to distinguish the distinct functions that language can have. As above, we don’t use language merely to assert. We utter sentences, in different grammatical moods, for different purposes. We might think that mental episodes, like sentences in language, also have functions that are usefully distinguished through their having something (at least) very similar to grammatical moods. Beliefs, for instance, might reasonably be thought to have an indicative function. We might take beliefs to have the function of indicating ways the world is and to fulfil this function by representing the world to be a certain way. Notice that I can express my belief that the coffee is hot by using language in the indicative mood; ‘The coffee is hot’, I might say. So too, many mental episodes with qualitative character, i.e. most mental episodes that are like something for us when we experience them, might reasonably be thought to have an indicative function. My perceptions, in particular, all seem to indicate ways the world is: my gustatory, visual, and auditory experiences seem to indicate that, e.g., my coffee is bitter, the leaves are green, and the birds are singing. We might think that they fulfil this indicative function by representing the world: they represent, respectively, the bitter coffee, the green leaves, and the singing birds. We might think that some of our other mental episodes, however, and even some of our other qualitative episodes—those episodes, recall, that it is like something for us to have when they are conscious— have a different function. Most relevant for our purposes is the idea that some of our mental episodes have an imperative function. Richard Hall (2008) introduced this idea, holding that some mental episodes have the

The Need for Complexity  57 function of motivating action and that they fulfil this function by commanding that the action be done. The bodily sensation of an itch, for his paradigm instance, has the function of motivating one to scratch and is to be explained by having a content which commands one to scratch. Many other qualitative states, like perceptions, don’t seem to motivate. Or, at least, they don’t seem to motivate by themselves. The taste of the bitter coffee perhaps indicates the way things are with the coffee, but it doesn’t, by itself, motivate me to do anything, e.g. to drink the coffee. Neither am I directly motivated by the sight of the green leaves nor the sound of the singing birds. But itch and other bodily sensations, we might think, do motivate directly and all by themselves. On Hall’s view, bodily sensations have a motivational function, and they fulfil this function by commanding the person who feels them to do something. The intentional contents of states with this imperative, motivational function might thereby be dubbed imperative contents. Having distinguished these moods, in returning to the orthodox assumption that pains are all and only those mental episodes with a distinctive qualitative character, we might now consider what might be the function of having mental episodes with this supposedly distinctive character. In particular, do pains have an indicative function or an imperative function? We might initially be tempted by the idea that pains have both of these functions. Perhaps, that is, pains have a dual function: both to indicate something and to motivate us to do something. According to our everyday theory, pains at least typically motivate behaviour— concerning both our bodies and the (at least, typically) unpleasant episode that I’m having when in pain. Call the former types of behaviours bodily directed actions and the latter experience-directed actions. The everyday reports and behavioural explanations we offer and accept in everyday life suggest that we accept that pain typically motivates behaviour of both kinds: I might say both that the pain in my hand made me pull it off the stove, and also that I took a Tylenol because of the pain. That pains, at least typically, also indicate something, however, is also a folk platitude. The everyday reports and behavioural explanations we offer and accept in everyday life at least suggest this: I might say that I can feel the pain in my tooth, that I can feel the burning of my hand, that I can feel I’ve sprained my ankle, and so on. Taking both kinds of platitudes at face value, we might make the further theoretical claim that pains have both an indicative and imperative function. It is apparently accepted by our everyday theory that pains both tell us about things and motivate us to do things. Hall himself (2008) adopted a hybrid view for pain according to which they have both an imperative and indicative function, and this dual functionality was to be explained by their having intentional contents which both represent and command. 22 For itch, by contrast, he

58  The Need for Complexity advocated a pure imperativism; itch has only an imperative function and an intentional content which commands one to scratch. According to Hall, itch doesn’t represent anything, it just commands you to do something. Pains, he thought, likewise have an imperative function to be explained by a distinctive intentional, imperatival content which commands one to take bodily directed action. But unlike itch, pains are taken by Hall to also have an indicative function to be explained by a distinctive intentional, representational content. On this view, pains both represent a distinctive condition of the body and motivate one to take a distinctive action directed at the body. As argued in the previous section, however, there is no plausible candidate for a distinctive condition of the body which correlates well with pain; there’s no distinctive condition of the body which pains might plausibly represent or have the function of indicating. A hybrid imperativism, like Hall’s, which assumes there is some such condition, will accordingly inherit those objections to representationalism from the previous section. 23 This remains true even if further, imperative, content is added. Indeed, the failure to identify a distinct class of bodily conditions which pains represent is offered by Colin Klein (e.g. 2015a) as a motivation for the pure imperativism he developed from Hall’s theory for itch. Klein stresses that to characterise the function and content of pain, we might look either to what causes it or to what it causes. Klein recognises that the causes of pain are too varied to plausibly posit a distinctive representational content with an indicative function, but he nonetheless holds that what pains cause are suitably unified to support positing a distinctive imperatival content with a motivational function. The imperativist and representationalist for pain have much in common. Both accept the orthodoxy: it is agreed that pains are all and only those mental episodes with a distinctive qualitative character, i.e. the pain quality. So too, they agree that qualitative character is explained by (or stronger: depends on, or even consists in) intentional content: the qualities of a mental episode are (at least) to be explained by what the mental episode is about. It should be kept firmly in mind that the imperativist claims that pains have the function not only of motivating but of motivating a distinctive kind of action; as per the orthodoxy, pains have a supposedly distinctive qualitative character and this theory, like representationalism, aims to explain it by positing a distinctive content. The core difference between these intentionalist views is in what they take the function of pain to be. According to the imperativist, pains do not indicate by representing that you’re in a distinctive bodily condition, instead they motivate by commanding that you take a distinctive bodily directed action. Unlike the representationalist, the imperativist about pain thinks that pains are not about the way the world is, but that they are instead about what is to be done.

The Need for Complexity  59 Klein begins his wonderfully written defence of pure imperativism (henceforth, merely imperativism) by making these commitments explicit and specifying the supposedly distinctive imperative content of pain (2015a, p. 1): In virtue of being pains, they [pains] have some common [qualitative] feature. … In what follows I will give an account of that common feature. I will argue that pains are imperatives. They are sensations [i.e. mental episodes with qualitative character] with a content, and that content is a command to protect a part of your body. … All pains have imperative content and that content is what distinguishes them as pains. Note that this is an imperativism for pain and not for affect, i.e. the unpleasant quality that pains paradigmatically have. The imperativist here (quite rightly) agrees with the representationalist in taking pain and affect to require distinct accounts. Even if we grant that pains have a motivational function, we might wonder whether having a content which commands that something be done can best explain this function. If not, then the core reason to accept imperativism is undermined. After all, we might think that my asking you to pass the coffee doesn’t have the function of motivating you to pass the coffee, but only a communicative function of something like expressing my desire that you pass the coffee. 24 For present purposes, however, let’s grant that if pains are commands to take a distinctive type of action, then they have the function of motivating that distinctive type of action. A second initial concern, which leads to my central argument against imperativism, arises from consideration of what pains are like for us from the inside when we turn our attention to them; in particular, consideration of whether when we are aware of our pain, we are aware of being commanded to perform a distinctive action type. Those who hold that qualitative character is (at least) explained by intentional content have tended to subscribe to an idea called the transparency thesis. According to this thesis, my mental episodes are transparent to me, such that when I attend to my mental episodes—when I consider them ‘from the inside’—what I become aware of are not features of those mental episodes themselves, but instead only what those mental episodes are about. When I have a visual experience of the blue sky, for instance, and turn my attention to this experience, I don’t become aware of the experience; I become aware of the blue sky. In general, when I attend to my experiences, I become aware of what they are about. Experience, like a pair of clean glasses, is ‘transparent’: I see right through it to the thing in the world which it represents. When I’m engrossed in a story, for another analogy, I cease to be aware of the squiggles on the page

60  The Need for Complexity and become only aware of what the story is about. That we ‘see right through’ our experiences to the world in this way is taken by many to be a reason for thinking that experiences are about the world in the first place. 25 Imperativists have offered a transparency thesis for pain in support of their view. Remember that they, like representationalists, think that pains are about the world, i.e. they have intentional content. One reason they offer for thinking this is true is that we see right through the episode to what it is about. Manolo Martínez (2015, 2269), for instance, urges that we should accept: …what we might call an imperative transparency thesis … Headaches direct us to do something about our head; toothaches to do something about our teeth; premenstrual cramps direct us to do something about our abdomen. Klein (2015a, p. 21) likewise alleges that when you are aware of the supposedly distinctive pain quality, “…you are aware (only) of a command, issued by your body, ordering you to take action”. To be aware of your pain, they allege, just is to be aware of the felt command. Klein and Martinez argue that while it’s true that transparency for pain fails for any representational content, it nonetheless holds for the posited imperative content of pain: when we attend to our pain, we aren’t attending to some distinctive way the world is, but we are attending to a distinctive command to do something. To be aware of the supposedly distinctive qualitative character of pain is to be aware of a distinctive action that I am being commanded to perform concerning my body. It is hard to adjudicate claims about what things are like from the inside, but my own introspection does not support these claims. When I introspect my pains, I am not always aware of a command ordering me to take any bodily directed action. And there is certainly no distinctive bodily directed action which I am always aware of being commanded to take upon introspection of all my pains. Here, as I sit, I twist the pen cap into my hand until it causes me pain, and turn my attention, as best I can, to that pain. I seem to be aware, in this case, of a slight burning feeling. I also, in this case, seem to be aware of my hand and how the skin feels. It is not clear to me, simply on the basis of this introspective exercise, how these feelings are related. It is clear to me, however, that I am not aware of any command, or urge, to protect my hand. None whatsoever. But I am aware of my pain. Examples from my own introspection proliferate. I invite you to consider for yourself: when you turn your attention to your conscious pains—i.e. the qualitative way they seem to you to feel when you are aware of them—does it seem to you that the only thing that you find is a command to take a bodily directed action? (If you find

The Need for Complexity  61 this at all.) And, moreover, does it seem to you that there is a distinctive type of bodily directed action you are aware of being commanded to take that is common across your pains? If the imperative transparency thesis is true, then whenever we attend to our pains from the inside, we should be aware of a command to take a distinctive type of bodily directed action. Imperative transparency for pain is not essential to the theory. If your introspection is like mine, that’s good for the theory.26 While the theory is supposed to receive support from the claim that what we are aware of when we are aware of our pains is a felt command to protect our bodies, the theory may be true even if this is false. Even if I don’t see “right through” my pains to what (if anything) they command, they may nonetheless command. Transparency is supposed to be an argument in favour of intentional explanations of qualitative character, but its failure doesn’t show that an intentional explanation fails. What does begin to raise a direct problem for the theory, however, are the wide range of actions which pains do seem to motivate when I introspect. Not only am I not aware of the urge to take a distinctive bodily directed action whenever I attend to my pain, but I am aware of a wide range of different urges when I attend to distinct pains. (And, as above, sometimes none at all.) The core problem for imperativism I want to press is that pains do not have the function of motivating a distinctive type of action. What pains cause, just as what causes pain, is too heterogeneous for pain to be adequately explained by a distinctive, intentional content. Even an imperative one. Pains neither indicate a distinctive bodily condition nor motivate a distinctive bodily directed action. The wide range of behaviours motivated by pain are not plausibly construed as any distinctive action type which pains might command. If that’s right, then imperativism fails. When evaluating imperativism, as when evaluating representationalism, we’ll again need to take care in specifying the intentional content— in this case, to take care in specifying exactly what pains are supposed to command. If we leave the type of action completely unspecified, then far too many non-pains will be deemed pain; if pains are just the felt bodily command to take any bodily directed action, then itch, hunger, thirst, and more will all be deemed to be pains. On the other hand, if we get too specific in the type of action we suppose pains to command, then some pains will be left out. The command had better not, for instance, be to withdraw a body part; while some pains might plausibly be construed as commanding one to withdraw parts of the body, others (e.g. headaches again) clearly cannot. Imperativists have of course recognised the need for care in specifying the posited content, i.e. in specifying the distinctive kind of action which pains supposedly have the function of motivating. Klein explicitly takes

62  The Need for Complexity the pains of recuperation—pains after damage and during which healing needs to occur—as paradigms when offering the above formulation. As it seems to me the most promising version of the view currently in the literature, we will use it to evaluate the theory. 27 That is, we will consider the idea that pains command one to protect a part of the body—and we are granting, as above, thereby have the function of motivating one to protect a part of the body. While I want to grant that at least some actions motivated by at least some pains are protective of the body, there are nonetheless a wide range of pains which cause a wide range of actions which are only implausibly described this way. If we try to expand the idea of what counts as a protective action to encompass all the actions caused by all the pains, we’ll end up deeming many things which aren’t pains to be pains. Imperativism, like representationalism, suffers from a glut of dissociative cases. In challenging the adequacy of the theory, let’s look first at three classes of actions motivated by pain, but that are not plausibly described as bodily-directed protective actions: experience-directed actions, bodilydirected actions which are not protective, and other-directed actions. In considering these cases, I will use some introspection. Introspection is not nothing: if your introspection is like mine, then you’ll be sceptical of imperativism. As noted, however, introspection is also not everything: people tend to find what they look for when attending to their own mental lives. Crucially, then, we can also look to behaviour, along with the reports and explanations of behaviour that we offer and accept in everyday life. We’ll use introspection, behaviour, and our everyday theory to consider all three problematic classes of action, before considering how the imperativist might respond. Consider the first class of cases: pains which motivate experiencedirected action. These abound. Consider a recurrent sinus headache. On day three of a nasty infection, when my sinus headache flares up, and I turn my attention to the pain, I seem to be aware of an urge, or command, to do something about the pain itself. I at least seem to myself to be motivated to do something about the pain itself, i.e. something about the experience that I am having. And it at least seems that I am motivated to do this by the pain. Moreover, my behaviour reflects the motivation that I seem to myself to have: when I feel the sinus pain, the action that I take in response is to imbibe something for the pain. Finally, I report my behaviour and accept the reports of others, as if the pain indeed motivates experience-directed action: “The pain was so bad, that I had to take something for it”, I say. The pains of those unfortunate enough to have phantom limb pain, mentioned above, seem an extreme but clear example of this kind of case. While they may try to protect the space the missing limb is felt to be, they are surely not taking action to protect the limb that they know is not there; rather, they seem to be trying to avoid pain. Their pain causes them to take experience-directed

The Need for Complexity  63 actions. Similarly, a person in chronic pain, convinced that there is nothing wrong with the felt place of their pain, may engage in a wide range of pharmacological, psychological, and behavioural techniques to manage the pain. Of this wide range of activities, few that I can think of seem at all plausibly targeted at protecting a body part. Though phantom limb and chronic pain are pathologies, they are surely pathological pains. Moreover, many cases of pain—like my sinus headache—seem to me accurately described this way. We at least seem to ourselves to be motivated by pain to take experience-directed action, this motivation is reflected in our behaviour, and we will give and take pain-based explanations of these experience-directed behaviours. Consider next the second set of cases: pains which motivate bodilydirected actions that are not protective actions. Recall the MPQ and the wide range of sensory descriptors used to describe the specific, sensory ways that a pain may feel: throbbing, burning, stabbing, dull, sharp, shooting, and so on. As noted above, the orthodox idea can encompass these by maintaining that there is a distinctive pain quality which is felt in these more fine-grained ways. On the imperativist story, these more fine-grained qualities are to be explained by some more specific protective actions that I am being commanded to take. 28 Klein gives a few examples (p. 98): Both fractures and sprains, for example, are frequently referred to as aching. … Fractures and sprains don’t have much physically in common, but they do require the same sort of protective action—that is, avoidance of weight-bearing and use. Cuts, fractures, and bruises are often described as hot or burning, suggesting proscription against contact. Some pains—such as cramping pains— obviously relate to the cessation of muscular activity. Not only does the distinctive pain quality correspond to the command to protect the body, but the more fine-grained qualities of pain are taken to correspond to commands to protect the body in more fine-grained ways. A first worry about this way of dealing with our second class of cases is that the fine-grained differences in sensory qualities do not seem to correspond well to fine-grained differences in motivated protective action. In particular, it seems that the fine-grained sensory qualities of my pains may differ dramatically, without any noticeable change in the bodily-directed actions that I am motivated to take. Both a dull and a sharp pain in my hand may motivate initial, tentative, exploratory touch and movement, followed by avoiding both use of the hand and contact with other objects. Gnawing or pricking pains in my foot, for another example, do not seem to correspond to any differences in bodily-directed actions. Or, at least, if they do, I have no idea what they are. Transparency, at least, seems to me to fail here. I am often unaware of being

64  The Need for Complexity commanded to take even subtly different protective actions, even when I am aware of radically different fine-grained qualities. ‘Avoidance of use’ is Klein’s own example of a protective action that pain may command, but notice that a wide range of pains with seemingly very different qualities will motivate this same action. Many pains thus seem to motivate the same or similar bodily-directed actions despite having dramatically different qualities. Set this worry aside, however, and consider what I take to be the central problem: whatever their more fine-grained sensory qualities, there are a wide range of bodily-directed behaviours caused by pains that are implausibly classed as protective in any way. Introspection, behaviour, and our everyday theory support these including, for instance, rubbing, pressing, holding, blowing, and more besides. Some pains cause me to crack my back, others to bend my toes, and others to suck my thumb. And on and on. One doesn’t typically think of this wide range of behaviours as protective, and it is often hard to plausibly describe them this way in context. If I get hit in the thigh by a softball and feel compelled to “walk it off”, it is odd to describe my action as protecting my leg. Hasn’t the damage been done? What am I protecting my leg from? Further damage? This seems implausible. Many pains of recuperation—the theory’s paradigm cases—seem to me this way; in many such cases, the actions I am motivated to take seem plausibly described as nursing or tending to bodily damage which has already occurred, not protecting my body from (yet further) damage. If I have a headache, I may feel compelled to drink lots of water and rub my temples, but neither of these seem to be protective of my head. In these many cases, motivation is present and is even bodily-directed, but the bodily-directed actions which are motivated don’t seem to be protective. So it seems to me, so I behave, and so we accept in our everyday reports and explanations. Consider finally the third class of cases: pains which motivate otherdirected actions. Though largely overlooked in contemporary, analytic philosophy, 29 these actions are a valuable part of the role that pain occupies in our everyday life. When in pain, I am often vulnerable and in need of help from others, and communicative action can facilitate the meeting of these needs. It seems to me that my pain sometimes motivates me to perform these communicative actions, e.g. to complain to others about it. This is how it seems from the inside, how I apparently behave, and is a behavioural explanation that we accept in our daily life. Perhaps the most obvious cases of other-directed actions which pain motivates are the actions motivated by the pain of infants. Pain causes infants to cry, and this crying plays a crucial communicative function. Of course, we adults also sometimes cry when in pain. Many of our own motivated reports and expressions of our pain seem to have the same important communicative function. If so, then some of the actions

The Need for Complexity  65 motivated by pain are neither experience-directed nor bodily-directed but are other-directed. Introspection, behaviour, and our everyday reports and explanations thus suggest that what pains cause is heterogeneous—including not only bodily-directed protective actions but also (at least) experience-directed actions, bodily-directed actions which are not protective, and otherdirected actions. How might the imperativist respond? It seems to me that for all the above cases they might maintain either that the actions are not actually caused by pains, or that the actions caused are actually bodily-protective actions. Consider first the suggestion that the actions are not actually caused by pain. This will be more plausible for some cases than others. Experiencedirected actions, for instance, are explicitly classed by the imperativist as belonging to this category. On this view, I am not motivated by pain to rid myself of pain (ever), rather I am motivated to rid myself of pain by unpleasant affect. It is the unpleasantness caused by being in pain, and not the pain itself, which motivates me to take experience-directed action. Going further, perhaps at least some of the actions in the other two classes above can also be redescribed in this way. Perhaps, for instance, it is not the pain which causes the baby to cry, but unpleasant affect. Perhaps when I engage in non-protective bodily directed actions, e.g. rubbing and pressing my aching muscles, I am not motivated by the pain I feel in those muscles, but by the unpleasant experience the pain is causing me to have. Now in our everyday life and in pain science (as we will see) we take the unpleasantness of pain, when it’s present, to be a component of the pain. My pain is, at least typically, unpleasant. The unpleasant experience that I am having is the pain experience that I am having. To supplant this, we would need a distinct clear story about the unpleasantness of pain, why pain at least typically causes an unpleasant experience, and how unpleasantness (and not pain) motivates the actions in the above cases.30 Let’s grant that there is a successful story to be told, and let’s even grant that affect can explain many of the intended cases. The bigger problem is that if we grant all this, there will be many cases of pain which then apparently do not motivate any actions whatsoever. Consider again my sinus pain. In this case, I seem motivated only to take experience-directed action. That is, the only actions that I seem to be motivated to take, that I actually take, and that I mention in everyday discourse as being motivated by the pain to take are actions aimed at ridding myself of the unpleasant experience that I am having. I feel no urge to, nor do I, take any actions directed towards my sinuses; indeed, I do not even know what protective actions towards my sinuses it might make sense to take. If we grant that these actions are not motivated by the pain

66  The Need for Complexity (it is affect instead which motivates them, we are granting), it seems that there are no actions motivated by the pain at all. If experience-directed actions are not motivated by the pain in this case, then none are. Cases like this generalise. If all of the experience-directed, otherdirected, and bodily-directed actions which are not protective that pains seem to motivate are instead granted not to be motivated by pain, then there are many pains which seem not to motivate any actions whatsoever. These include not only recurrent pains like my sinus pain, phantom limb pain, and chronic pain, but headaches of all kinds, visceral pains, and many more besides. If the infant is caused to cry not by pain, but by affect, then their pain apparently does not cause them to do anything at all. There are a glut of humdrum, everyday cases where the only actions that we seem caused to take are experience-directed, bodily-directed but not protective, or other-directed. If we deny that these actions are caused by the pain, then a great many pains apparently do not motivate at all. The very idea that pains have the function of motivating action (much less of a distinctive type) is then undermined. I take it that imperativists will claim that I am motivated by my pain to protect my body in all these cases—even if I am also motivated by something other than my pain (e.g. affect) to take yet additional actions (e.g. eliminate the pain). Surely, they might say, I am motivated to protect my sinuses when I feel pain there. Well surely, I want to say back, I don’t want to protect my sinuses any less than normal. I have a standing desire to protect my body parts. Protecting my body is something that I always want to do. If you threaten my sinuses or move to act against them, I will move to protect them. My sinus pain, however, seems to have nothing to do with this. No additional bodily-protective actions are caused or motivated by the sinus pain. Ditto, it seems to me, for the wide range of cases mentioned above. This consideration brings to light that pains, according to pure imperativism, are supposed to be explained as having the function of motivating actions which I already have a standing motivation to perform—namely, to protect my body. Protecting my body is something that I am always motivated to do, whatever else I might be experiencing. Klein, moreover, takes pains themselves to be standing imperatives. He writes (p. 61), “It [the pain] is an imperative that remains in force as long as it continues to be issued and until it stops”. So, I have a standing care and concern for my body which will motivate me to protect my body when I register that it is threatened—with or without pain. And according to the theory, when in pain, I have an additional standing imperative to protect my body, posited to explain why I am motivated to protect my body. This is, at least, odd. The oddness here becomes pronounced when we consider Klein’s explanation for pain asymbolia. As described above, the pains of the asymbolics apparently fail to motivate. Klein argues that what the asymbolics

The Need for Complexity  67 lack is the capacity to care about the body. Because they do not care about their body, they fail to be motivated by pains’ commands to protect it. He writes (2015b, 500): Pains motivate because we care about our bodies. If we were to stop caring—something that’s ordinarily impossible, for good biological reasons—then pains wouldn’t matter. Asymbolics are a realisation of this unusual possibility. Care is here an enabling condition of pain’s motivational force. But care, note, is itself a motivational state. If I care about my husband, then when I am informed that he is threatened, my care will motivate me to protect him. I do not need any further standing state to be motivated to take husband-directed action. Let us grant that it’s care about the body which asymbolics lack and I have. What they are lacking is a standing motivational state to protect their bodies, but they aren’t lacking pain. Pains are not only being posited as motivating actions which I already have a standing motivational state to perform (namely, care about my body), but if I lack this other standing motivational state, then pains won’t motivate. If that’s right, then pains don’t seem to be doing the work in explaining my motivation to take bodily-directed protective actions when my body is threatened—rather, my concern for my body is. My concern for my body will motivate me to protect it whether or not I am in pain, and if I lack that concern, my pain will not motivate me.31 In summary of the first option for dealing with our three types of problematic cases: if the imperativist denies that pain motivates the wide range of experience-directed, bodily-directed but not protective, and other-directed actions which we typically take them to motivate, then there will be a glut of pains which do not seem to motivate any action whatsoever. In a great many cases, it does not seem from the inside as if we feel any distinctive urge to protect our bodies and we neither take nor report any such motivated actions. Of course, it is not as if we are not at all motivated to protect our bodies when we undergo these pains: we are always motivated to protect our bodies. Most all of us care about our bodies and thus have a standing motivation to protect our bodies. These pains, however, add no further motivation to protect the body in a wide range of cases, e.g. headaches, visceral pain, and so on. Going further, given that we already have a standing motivational state to protect our bodies—one which is accepted as necessary for me to be motivated to take any bodily-directed protective action even when in pain—it’s become difficult to see what motivational role the theory has left pain to play. Consider, then, the second option for dealing with our three types of problematic cases: the suggestion is that the wide range of actions that pains seems to cause are all bodily-directed protective actions.

68  The Need for Complexity This is more plausible for some of the actions discussed than others, and it is implausible in a great many cases. For experience-directed actions, this suggestion is flatly incredible. I do not, for instance, take aspirin to protect my foot. Instead, as above, imperativists explicitly take the first option for such actions, and claim that these actions are caused by something other than pain. Perhaps other-directed actions, however, are more plausibly described as bodily-directed protective actions. Perhaps the baby cries to protect their head—by getting someone else to protect it! Perhaps, that is, pain communication itself has a protective function. Note, however, that pain communication elicits a wide range of actions from others. Are the compassion, comfort, and general help which my loved ones (and good professionals) offer, upon my communicating my pain, all bodily-directed protective actions? Is my motivation, in communicating my horrendous toothache, to get my friend to hug me? Is my friend’s hug, in response to this communication, an action which somehow protects my back? The protection of body parts seems to me a very small subset of the otherdirected actions which pains motivate. Most problematic for the theory, however, are the many bodilydirected actions seemingly caused by pain which seem not to be protective. As above, if we class all of these as caused by something other than pain, then there will apparently be a glut of cases in which pains cause nothing at all. But might we instead class them as protective, and caused by pain, after all? Might protective actions include not only actions like limiting motion and avoiding contact (the paradigm protective actions emphasised by Klein) but actions like weight-bearing, rubbing, and stretching?32 To accommodate all bodily-directed actions caused by pain as protective would require an expansive extension of ‘protective’ which far exceeds our everyday understanding of the term. Consider, for instance, what Klein says about menstrual pain. He notes (2015a, p. 115), “The imperative that constitutes them is roughly the same sort as the imperatives of childbirth—something about protecting the uterus, say”. Notice first that the bodily-directed actions that one is caused to take when suffering menstrual pain and labour pain are dramatically different, despite supposedly being explained by the body issuing the same command. In labour, especially at its latest stages when pain is most intense, one is apparently motivated by the pain to push. Is pushing an action which protects the uterus? It seems a bit strange to say so, but perhaps; when pushing, I am ridding my body of something that would cause damage were it to remain. Menstrual pain, however, apparently motivates one to take a range of other bodily-directed actions, including, e.g., rubbing and massage. Are these also ways of protecting the uterus? It seems a stretch to say so. If these actions are not accepted as being motivated by the

The Need for Complexity  69 pain, then it again seems that the pains motivate no action whatsoever. No others, at any rate, are typically introspected, caused, or reported. The biggest concern for accepting an expansive notion of protective action, however, is that (at least) many of the bodily-directed actions caused by our other bodily sensations will be included. When I am tired, I am motivated to sleep; when hungry, to eat; when itchy, to scratch; and when nauseated, to purge. Sleeping, eating, scratching, and purging, however, are as protective as pushing, limiting motion, or cradling. If the mother’s pushing, the infant’s crying, the burned’s rubbing, and the bruised’s stretching are all protective actions, then there seems no principled reason not to include scratching, eating, drinking, and purging. In short, it seems that all homeostatic sensations cause bodily-directed actions which are as protective as many of the bodily-directed actions which pain causes.33 If so, then we have not yet identified the distinctive content that was supposed to explain the supposedly distinctive qualitative character of pain. These other bodily sensations, with their other qualitative characters, would have the same identified imperatival content. To further highlight this difficulty, consider once more the explanation that Klein offers for pain asymbolia. On this view, asymbolics lack care about their bodies, such that commands to protect their body fall on unmotivated ears. But notice now that asymbolics are still motivated by their other bodily sensations. And these, too, are supposed to be explained by felt bodily commands. They itch, eat, drink, and—it seems—follow all the other commands we might grant to explain homeostatic sensations. If lacking care of the body results in their failing to be motivated by the body’s pain commands, why not these others? Klein says that the commands which explain pain all concern direct threats to bodily integrity, whereas the commands which explain other homeostatic sensations concern only indirect threats. In seeming contradiction to the suggestion in the passage quoted above, then, asymbolics do not entirely lack concern for their bodies. Apparently, they lack the capacity to care about direct threats, but retain the capacity to care about indirect threats.34 But this distinction between direct and indirect threats does not align with the distinction between pains and other homeostatic sensations. Many of the causes of my homeostatic sensations are direct threats. I may become itchy (i.e. on an imperatival view: undergo the felt command to scratch) because my skin has come into contact with a toxin. Isn’t this a direct threat? If not, why not? On the other hand, many pains apparently concern only indirect threats, e.g. when I have a headache or a stomachache. There are, so far as I can tell, often no direct threats in these situations. Or at least, low nutrient levels (as in hunger) seem to me as direct a threat to my bodily integrity as a burn in the process of healing (as in pain). Examples proliferate.

70  The Need for Complexity Let’s take stock. I’ve been arguing that not only the causes of pain, but what pain causes is massively heterogeneous. I’ve been using introspection, behaviour, and our everyday theory to argue that these include (at least) experience-directed actions, other-directed actions, and nonprotective bodily-directed actions. The imperativist might respond by saying either that these actions are not really caused by pain or that they really are actions which protect the body. If these actions are not really caused by pain, however, then there are a lot of pains which apparently don’t cause anything. If, on the other hand, these actions are really protective, then the theory seems unable to distinguish between pains and other homeostatic sensations like itch, hunger, or thirst. Indeed, some of the bodily-directed actions caused by these other homeostatic sensations seem much more plausibly classed as protective than some of the bodilydirected actions caused by pains. We have been evaluating the theory by focussing on the command to protect the body, and an obvious way that an imperativist might respond to the above criticism is by altering the claim about what pains command. Perhaps pains have the function of motivating some other distinctive type of action, and the felt command to take this action can explain their supposedly distinctive qualitative character. Klein claims (2015a, p. 68) that “[t]he advantage of protection imperatives … is that protection imperatives command a straightforward relatively unified type of action”. But if what I have here been arguing is correct, then the class of protective actions is not a very unified action type. Indeed, if we consider the wide range of actions we take to protect other things that we care about, e.g., our children, our property, our ideas, and so on, the class of actions which may count as protective of an object (or a body) is apparently highly varied. Maybe another type of action could do better. But what distinctive type of action might pains instead command? It’s far from obvious. Notice that it is obvious in the case of the other bodily sensations on which the theory of pain is built. When I feel an itch, there is no ambiguity about the distinctive type of action that I feel compelled to take. While there is flexibility in how and when I scratch, there is no uncertainty that to scratch is what I feel motivated to do. Similar considerations seem to me to apply to thirst (to drink), hunger (to eat), and so on. I may develop some pathological condition such that when I feel these sensations, I know they are to be resisted, and I may then be motivated to rid myself of the sensations. If I come to know that I have a pathology which makes me feel thirsty when I don’t need to drink, for example, I may begin to take actions to rid myself of the useless thirst. Even in these cases, however, there is no doubt—using introspection, behaviour, and everyday theory—that the action which thirst motivates is to drink. For pain, however, it seems that a wide range of heterogeneous actions are motivated: a wide range of experience-directed, other-directed, and

The Need for Complexity  71 bodily-directed actions. No distinctive unified action type is transparent or obvious. In hopes of identifying a distinctive unified action type, and thus a distinctive imperatival content which can explain pain, an imperativist may look to pain science. Remember, the core argument that pains command action is that motivating action is what pains are for. Perhaps pains have the biological function of motivating a distinctive action type as determined by the workings of a distinctive biological pain system. If a distinctive biological pain system were identified, then all seeming counterexamples to the theory may be explained as malfunctions of this system. Is this credible for imperativism for pain? As noted in the introduction, most philosophers of pain presume that there is a pain system and that there would be times when it fails to function optimally or be in an optimal environment. As Klein writes (2015a, 118), “…the idea is that the pain system is constructed so as to produce imperatives that promote well-being in most cases, mostly reliably, in most circumstances, for most people. It is liable to malfunction, as is any biological system”. Imperativists already sanguinely accept that there will be a wide range of maladaptive pains, i.e. pains which issue commands are not beneficial, adaptive, or useful to receive. All the commands constantly being ‘issued’ by your body, but which you have already obeyed or which are impossible to obey, for instance, are useless and maladaptive. Martínez (2015) dubs those pains which are ‘irrelevant, unduly insistent, overly predictable, etc.’ as spammy pains, and he admits there are many of these. If we think about things from an evolutionary perspective, a glut of maladaptive pains may be unsurprising. We might think it’s much more evolutionarily advantageous to be motivated, e.g. to protect our bodily integrity, even when it isn’t threatened, then to fail to be motivated to protect our bodily integrity when it is threated. As we noted when considering representationalism, it may be best, from an evolutionary perspective, that we have a glut of ‘false positives’. One thing needed for this move to work is that we must not have too many maladaptive pains; pains must be adaptive often enough for the posited function to be credible. The link needs to be strong enough that the explanation is plausible. As Klein recognises (2015a, p. 119): What helps survival is to have a pain system that more or less reliably commands us to protect ourselves in cases where protecting ourselves promotes bodily integrity. That system doesn’t have to be perfectly reliable to be useful. Further, it is only because there is a determinate sense in which the pain system conduces to survival that we are able to talk about pathological pains as malfunctions… Of course, as pain limits movement and so imposes a survival cost, we should expect unnecessary pains to be more rare than [as an

72  The Need for Complexity example of another system with a lot of false positives] unnecessary eye-blinks—that’s why misfires such as paper cuts strike us as odd cases. Now it seems to me that far too many pains would be considered maladaptive or malfunctions for imperativism for pain to remain credible. Paper cuts (which do not seem to me to be pathological) aside, there are far too many pains which do not motivate actions of any distinctive type for us to simply dismiss them all as malfunctions or maladaptive. As above, a great many of my pains motivate experience-directed or other directed-behaviour. And the latter, in particular, seems adapative— consider again the infant’s cry. A great many of my pains also command me to do things that I have already done or about which I can do nothing further: headaches, toothaches, somatic and visceral pain, and more. Consider even the paradigm cases for the theory: recuperative pains. Pain persists far beyond my taking any bodily-directed actions which might be useful. Laid up in bed, while healing, there is no (at least no further) useful action that I can take to protect my body, but pain persists. Most all of my recuperative pains are apparently then maladaptive and ‘spammy’. In short, it thus seems to me that only a very few of our pains might be plausibly construed as useful commands to take any distinctive bodilydirected action. When we note again that we already have a standing motivational state—concern for our bodily integrity—which motivates bodily-directed protective behaviour whenever we register threat or damage, the functional claim looks even further unsupported. Very few pains apparently motivate bodily-directed protective behaviour, and we have another standing motivational state which does. A second and equally crucial thing needed for this explanation to work, however, is that there needs to be a pain system. But what is this system and what exactly is its function? It’s not protecting bodily integrity; as above, all homeostatic processes seem to have this function. And as above, adding the qualification that the relevant threats are direct does not seem to help; many homeostatic sensations besides pain are apparently responses to threats which are as direct. Klein often appeals to A.D. Craig’s homeostatic theory of pain, and we will consider this model in the next chapter. As I’ll there argue, Craig’s model—on which Klein heavily draws—fails to identify a pain mechanism or pain system, as against a homeostatic system. No distinctive function, or system, for pain is there identified. It’s not clear to which alternative system—and its supposed motivational function—an imperativist may appeal. I directly argue in the next chapter that there is no pain mechanism or system. Not only is there no pain mechanism or system yet discovered, I argue that what we have discovered gives us good reason to think there isn’t one. Appealing to the workings of a pain system to explain all

The Need for Complexity  73 seeming counterexamples cannot help the imperativist any more than it could help the representationalist, since there is no such system. The core problem for imperativism is that pains do not have the function of motivating a distinctive type of action. Again: what pains cause, just as what causes pain, is too heterogeneous for pain to be adequately explained by a distinctive, intentional content. Pains neither indicate a distinctive bodily condition nor motivate a distinctive bodily-directed action. The wide range of behaviours motivated by pain are not plausibly construed as any distinctive action type. If we widen the type of action to try to include them all, then too many non-pains will be deemed as pains. Appealing to a pain system to help identify a plausible action type will also fail, since, as I’ll argue directly in the next chapter, there is no such system. If that’s right, then imperativism fails. Recall that imperativism for pain was explicitly developed as a way to rescue intentionality for qualitative character from the concerns about representationalism for pain. I note again that rather than maintain that there must be some distinctive intentional content for pain, since there is some distinctive qualitative character all and only pains have, an intentionalist about qualitative character might simply reject the orthodoxy of simplicity. If the pain quality does not exist, then it needn’t be accounted for by the intentionalist—either by positing representational or imperatival content. Rejecting the orthodoxy of simplicity is an alternative that I urge the committed intentionalist to consider.

2.5 From the Pain Quality to a Pain System Contemporary, analytic philosophical theorising about pain begins with the starting assumption that pains are all and only those mental episodes with a distinctive qualitative character. Theories of qualitative character are then tested against pain. At the moment, the dominant theories of qualitative character are intentionalist—according to these theories, qualitative character is explained by (or stronger: depends on or even just consists in) intentional content. When mental episodes are like something for you, what they are like is (at least) explained by what they are about. I’ve argued in the previous two sections that the currently dominant, intentionalist theories of qualitative character are inadequate for explaining pain. Pains do not plausibly represent a certain bodily condition or command a certain bodily-directed action; they are too poorly correlated with any distinctive bodily condition or the motivation to take any distinctive bodily-directed action for these theories to be plausible. In trying to make these theories adequate, too many pains are left out or too many non-pains are deemed pains. As both what causes pain and what pain causes are massively heterogeneous, I submit that any other

74  The Need for Complexity intentionalist theory of the supposed pain quality that we might offer will continue to flounder. One might hold on to the philosophical orthodoxy and think that all this shows is that the currently dominant intentionalism theories are themselves inadequate; the problem isn’t that there is no pain quality, but that we need a better theory of the mental qualities. I submit, however, that no theory of pain which begins with the orthodoxy of simplicity will succeed for the simple reason that pains are not so simple. The idea that there is a distinctive qualitative character in virtue of which all and only mental episodes are pain is not reflected in either everyday life, science, or medicine. Instead, everyday theory—as we’ve seen in the last chapter—recognises that pains have many dissociating paradigmatic features. A paradigmatic pain involves damage to the body, registration of that damage, evaluation of that damage, an unpleasant feeling, the motivation to do something about both the unpleasant feeling and the damage, and perhaps more besides. Philosophical theories, however, in taking pains to be a distinctive qualitative character have typically privileged some single one of pain’s paradigmatic components to explain that supposedly distinctive qualitative character. If they do, they will continue to face a glut of dissociation cases: (1) episodes accepted by everyday theory as pains, but which lack that component; and (2) episodes which have that component, but which everyday theory does not countenance as pains. All such cases are unproblematically acceptable when we recognise that pains have multiple components, no one of which is necessary or sufficient. Cases lacking the representation of any particular bodily condition or motivation to take any particular action are then unproblematic. Pains which are not unpleasant, which motivate other-directed behaviours, and which dramatically vary in their sensory qualities are all unproblematically accepted as pains—even as they are already accepted in everyday life and the clinic. Notice that refusing to privilege some one of pains’ paradigmatic components does not require denying the existence of any of them. A componential account of pain can respect the fact that pains are paradigmatically qualitative, indicative of bodily disturbance, motivate behaviour (bodily directed, experience-directed, and other-directed), and more. I want to maintain with everyday theory that pain typically has all these features. That each of these components is a paradigmatic component of pain is what makes the theories which privilege some one of these components initially seem plausible. We can appreciate that one thing that pains usually do is indicate that our bodies are damaged. This makes tempting the idea that indicating some particular condition of the body is what pains are for. Similarly, we can appreciate that one thing that pains usually do is motivate us to do things. This makes tempting the idea that motivating some particular kind of behaviour is what pains are for. A multidimensional

The Need for Complexity  75 account of pain, however, can retain these facts without falling into these temptations—temptations which, as we’ve seen, have problematic consequences. Recall again, furthermore, that no reason is offered for accepting the orthodoxy of simplicity; as far as I can tell, the orthodoxy of simplicity is a mere stipulation which nonetheless currently constrains analytic philosophical theorising. I attempted to give an introspective argument for it, but—once the pain quality is appropriately distinguished from sensory and affective qualities—my own introspection does not support it. It is not justified by appeals to everyday theory. Armstrong explicitly recognised our everyday notion of pain to encompass, at least, two dissociating components. Klein notes that his own usage of the word ‘pain’—as picking out all and only those mental episodes with a supposedly distinctive quality—may be ‘the least common’ usage of the word in everyday life (2015a, pp. 10–11). I am not sure that we ever use ‘pain’ to refer to any such quality in everyday life. Pains, as posited by our everyday theory, are apparently a much wider and diverse class than they are stipulated by the orthodoxy to be.35 Stipulations, however, have their place. They are useful for all sorts of specialised purposes, including many philosophical explorations. Define your terms—in any intelligible way you may wish—and off to theorise you may go. Further, philosophers also often take one of their useful roles to be regimenting everyday theory.36 This may involve revising our everyday notion to clear up inconsistencies, disambiguating our everyday terms, solving the puzzles raised by everyday theory, and so on. In particular, regimenting our everyday theory can help us to more successfully explain and predict the posits of that theory—and, perhaps at the limit—to determine that some of the posits of our everyday theory don’t actually exist. Though the orthodoxy of simplicity apparently takes pains to be a much narrower class than everyday theory, perhaps regimenting our everyday theory in accordance with the philosophical stipulation would have benefits. Note well that the orthodoxy of simplicity would indeed require major revision of our everyday theory. So much revision is required that it is not clear to me that philosophical theories of pain, offered in according with this stipulation, are even theories of the same thing that we refer to using ‘pain’ in our everyday theory. Perhaps it is a theory of the same thing, however, and perhaps if we revised our everyday theory to match the philosophical stipulation, then we would gain predictive and explanatory power concerning pain. On the contrary, it seems to me that the very promiscuity of our everyday notion of pain contributes to its utility for everyday purposes. So I am, at the very least, sceptical. Those wishing to stipulate that pains are all and only those mental episodes with a distinctive qualitative character, i.e. the pain quality, should at least provide some reasons for thinking the major

76  The Need for Complexity revision to our everyday theory entailed by accepting this stipulation is worthwhile. The most obvious reason for revising everyday theory, and a good reason to do so, is to better align with scientific theory. If our everyday theory clashes with our best science, then we should revise our everyday theory. I wholeheartedly endorse this naturalist methodology. As we’ll see in the next chapter, however, our best pain science, like our everyday theory, recognises that pain is a multidimensional experience with multiple, dissociating components. Pain science yields no support for the supposed pain quality. Indeed, we might wonder whether the pain quality is even consistent with not only everyday theory but our best science. How might pain have the many dissociating components acknowledged by our everyday theory and our best science, yet also be all and only those mental episodes with a distinctive quality? One way would be if the supposed pain quality were just realised by these different components, in different combinations, by the activity of different systems, and on different occasions. Perhaps, that is, we can retain the orthodoxy of simplicity, but refuse to privilege any one of pains’ paradigmatic components nevertheless. Maybe all that the science of pain captures are the different neural, chemical, and biological mechanisms (differently) involved in (different) pain experiences, but all pain experiences nevertheless have a distinctive qualitative character. One worry with this proposal is that different components would always constitute the same quality, no matter their combinations. That’s at least odd. Another worry is that this would apparently make the scientific story about the pain quality rather different from the naturalist stories about any of our other mental qualities. The colour qualities of our visual experiences, for instance, are typically, when naturalistically explained, explained by the activity of the visual system. Similarly for the qualities of all of our other perceptions and sensations. It would be at least surprising if there were a distinctive quality which was realised by the workings of multiple distinct systems and mechanisms. Perhaps, however, one could deny that the dissociating components of pain are explained by distinct systems and mechanisms. For all I’ve presented so far, perhaps all of pains’ paradigmatic features—damage and its registration and evaluation, unpleasant affect, the motivation to do something about the unpleasant affect, the damage and its registration and evaluation, and perhaps more besides—are all explained by the workings of some one distinctive pain mechanism or system. Yet again, then, if there is a pain system, perhaps it could help the orthodoxy. Murat Aydede and Matthew Fulkerson (2014, 2019) have forcefully advocated a psychofunctionalist view of pain, intended to capture the complex, multidimensionality of pain, and taken to be explained by the

The Need for Complexity  77 workings of a presumed unified pain system. According to psychofunctionalist views, very roughly, we can (at least) explain different types of mental episodes by thinking about their different functions. Typically, psychofunctionalism is taken to be compatible with intentionalist theories: as we already saw above, we might think that the best way to explain what a mental episode is about is to figure out that episode’s function. But Aydede and Fulkerson advocate a psycofunctionalism that doesn’t posit any intentional content to explain the supposed pain quality. Instead, they think that content is irrelevant to the functions that pains play, such that we can better explain pain by appealing directly to the way the presumed pain system functions. Against intentionalist theories, they argue that no intentional contents are explanatorily needed and that their introduction instead creates problems. They are explicit that the details of the workings of the presumed system, and how exactly it will explain the function of pain, await further scientific progress. The adequacy of psychofunctionalism requires a pain system: it’s the workings of the presumed pain system which are supposed to explain the supposed pain quality. As we’ve seen, many philosophers of pain have, I think, likewise simply assumed not only that pains are all and only those mental episodes with a distinctive qualitative character, but that there is a distinctive pain mechanism, or system, whose workings might (at least) explain that qualitative character. As Klein rightly notes (2015a, p. 27), “Philosophical theories presuppose a theory about the biological role of pain”. They then go looking for (or simply assume that there is) some biological system whose working fulfils that biological role. Pain is supposed to be an unproblematic natural, biological kind to be explained through the workings of a natural, biological system. As we saw in the previous sections, if there is such a system, we could perhaps appeal to it for explaining the seeming counterexamples to either of the intentionalist theories. Psychofunctionalism for pain more directly requires the existence of a pain system which has the posited functions. Perhaps the multiple, dissociating components of pain can be explained by the workings of this supposed system. To settle these questions and evaluate a non-intentionalist psychofunctionalism for pain, we must turn to pain science. In the next chapter, I argue directly that we know enough now to justifiably conclude that there is no pain mechanism or system. What, in closing the current chapter, might we say about the philosophical orthodoxy of simplicity? First, it is unmotivated; no arguments are offered for it and the revisions of everyday theory that its acceptance would require are of dubious benefit. Second, it is inconsistent with the theories of qualitative character currently dominating analytic philosophy, i.e. naturalist, intentionalist ones. Third, as we’ll see in more detail in the following two chapters, it is apparently at odds with the componential accounts of pain accepted by everyday theory, our best science,

78  The Need for Complexity and clinical practice. Identification of a pain system could perhaps yield resources to deal with all of these difficulties. I’ll argue directly in the next chapter, however, that there is no such system. Though most analytic philosophers begin their theorising with the unquestioned assumption that pains are all and only those mental episodes with a distinctive qualitative character, this assumption should be rejected. I hope I have at least provided some strong reasons to question this assumption and the currently dominating theories which begin with its acceptance. Philosophers of pain can do better.

Notes







The Need for Complexity  79 the text, unless it’s explicitly employed by a view being discussed, to avoid confusion or further complication. None of the arguments in the text seem to me to turn on this particular word or anything which one might use it to reference. 12 There is some debate, among representationalists, about whether qualitative character is always (or necessarily, or essentially) conscious. Whether, as I might phrase the issue, the qualitative character of a mental episode is always something that a person who is having a qualitative mental episode is aware of. Higher-order representationalists about consciousness think not. On these views, for a mental episode to be like something for me, I must represent a mental episode (which represents the world) to myself. On these views, my visual perceptions may have colour qualities in virtue of the way they represent the world, but these perceptions will only be conscious—they will only be experienced, or be like something for me—if I represent the qualities of those perceptions (which themselves represent the qualities of the world). Armstrong himself adopted just such a higher-order theory of consciousness. First-order representationalists about consciousness, however, are currently more popular. On these views, the qualitative character of the mental episode which represents the world is always (or necessarily, or even essentially) conscious. Qualitative character just is a matter of what things are like for me. Thus, on first-order views, not only do mental episodes have e.g. colour qualities in virtue of what or how they represent the world, but the episode is like something for me in virtue of those very same qualities. As above in text, whenever disambiguating is required, I’ll use ‘phenomenological character’ to refer to conscious qualitative character. With this usage: according to a first-order theorist, all qualitative character is phenomenological character.



20 Interoception seems to me to be the most plausible candidate for the kind of representation of tissue damage to which the representationalist might

80  The Need for Complexity appeal. More technically put, interoceptive processing seems to me to be the best candidate for the relevant “mode of presentation”, as some philosophers may put it. The claim that pains are interoceptive, however, is itself controversial from the point of view of pain science. We’ll see some of this controversy in the following chapter, but compare, for instance Strigo and Craig (2017) and Price (2017).

22 Though note that the term ‘imperativism’ was coined by David Bain (2011). 23 Manolo Matinez’s (2011) hybrid view, for instance, will suffer from this. 24 For further discussion of whether imperativism can explain the motivational role of pain on which it is centred, see e.g. Bain (2011) and Aydede and Fulkerson (2019). 25 For the original version of this argument, see Harman (1990). 26 This seems to me to be so even if, as Aydede (2019) argues, there are versions of intentionalism that entail versions of transparency.

28 Or, for some qualities, the frequency or “pattern” in which I am being commanded, e.g. throbbing. See Klein (2015a) for the distinction between pattern qualities and other of pains’ sensory qualities. For reasons of space, I set these issues aside. 29 But see, for instance, Helm (2007) or Langland-Hassan (2017). 30 There are worries about why, if imperativism is true, pains are (so often) unpleasant. Why should it be so unpleasant to be commanded to do something to protect your body? This is especially puzzling since it’s evolutionarily advantageous to receive and follow these commands. The answers currently offered (e.g. Martínez, 2015) appeal, ultimately, to the way that pain disrupts agency. Pain often causes unpleasant feelings because it conflicts with my other goals and desires, or because I am being constantly commanded to do something that I don’t want to do. On its face, this is a rather odd story. As a single case, consider that, on an occasion, I may well want to lie in bed and do nothing—the very thing my pain commands. My pain may still be intensely unpleasant. Is it intensely unpleasant because I am constantly being commanded to do something that I am already doing? Why, then, are other pains whose commands I am also satisfying (e.g. the current, slight ache in my hip) not nearly so unpleasant? Perhaps there are answers here but I do not know what they might be. 34 The implied biological claim—that the capacity to care about indirect threats may remain intact while the capacity to care about direct threats breaks down—seems to me implausible and at least in need of support. But set it aside.

The Need for Complexity  81

36 See e.g. Quine (1960).

References Armstrong, D. M. (1962a). Perception and the physical world. Humanities Press. Armstrong, D. M. (1962b). Bodily sensations, vol. Studies in philosophical psychology. Routledge & Paul Humanities Press. Aydede, M. (2019). Is the experience of pain transparent? Synthese, 196(2), 677–708. Aydede, M., & Fulkerson, M. (2014). Affect: Representationalists’ headache. Philosophical Studies, 170(2), 175–198. Aydede, M., & Fulkerson, M. (2019). Reasons and theories of sensory affect. Philosophy of Pain 27–59. Bain, D. (2011). The imperative view of pain. Journal of Consciousness Studies, 18(9–10), 164–185. Bain, D. (2014). Pains that don’t hurt. Australasian Journal of Philosophy, 92(2), 305–320. Bain, D. (2017). Evaluativist accounts of pain’s unpleasantness. In Routledge handbook of philosophy of pain, J. Corns (ed.). Taylor & Francis Group, 40–51. Berthier, M., Starkstein, S., & Leiguarda, R. (1988). Asymbolia for pain: A sensory-limbic disconnection syndrome. Annals of Neurology: Official Journal of the American Neurological Association and the Child Neurology Society, 24(1), 41–49. Bond, M., & Breivik, H. (2004). Why pain control matters in a world full of killer diseases. Pain Clinical Updates, 12(4), 1–4. Brand, P. W., & Yancey, P. (1997). The gift of pain: Why we hurt & what we can do about it. Zondervan Publishers. Corns, J. (2014). The inadequacy of unitary characterizations of pain. Philosophical Studies, 169(3), 355–378. Corns, J. (2015). The social pain posit. Australasian Journal of Philosophy, 93(3), 561–582. Corns, J. (2018). Recent work in pain. Analysis, 78(4), 737–753. Correia, F., & Skiles, A. (2017). Grounding, essence, and identity. Philosophy and Phenomenological Research, 98(3), 642–670. Craig, A. D. (2003). Pain mechanisms: Labeled lines versus convergence in central processing. Annual Review of Neuroscience, 26(1), 1–30. Cutter, B., & Tye, M. (2011). Tracking representationalism and the painfulness of pain. Philosophical Issues, 21, 90–109. Devitt, M. (2008). Resurrecting biological essentialism. Philosophy of Science, 75(3), 344–382.

82  The Need for Complexity Fine, K. (1994). Essence and Modality: “The Second Philosophical Perspectives Lecture”. Philosophical Perspectives, 8, 1–16. Freeman, W., & Watts, J. W. (1950). Psychosurgery in the treatment of mental disorders and intractable pain: In the treatment of mental disorders and intractable pain. CC Thomas. Frances, A., & Gale, L. (1975). The proprioceptive body image in self-object differentiation: A case of congenital indifference to pain and head-banging. The Psychoanalytic Quarterly, 44(1), 107–126. Grahek, N. (2011). Feeling pain and being in pain. MIT Press. Hall, R. J. (2008). If it itches, scratch! Australasian Journal of Philosophy, 86(4), 525–535. Harman, G. (1990). The intrinsic quality of experience. Philosophical Perspectives, 4, 31–52. Helm, B. W. (2001). Emotions and practical reason: Rethinking evaluation and motivation. Noûs, 35(2), 190–213. Helm, B. W. (2007). Emotional reason: Deliberation, motivation, and the nature of value. Cambridge University Press. Hill, C. (2017). Fault lines in familiar concepts of pain. In The Routledge handbook of philosophy of pain, J. Corns (ed.). Taylor & Francis Group, 60–70. Inanici, F. F., & Yunus, M. B. (2004). History of fibromyalgia: Past to present. Current Pain and Headache Reports, 8(5), 369–378. Kripke, S. (1980). Naming and necessity. Harvard University Press. Klein, C. (2007). An imperative theory of pain. The Journal of Philosophy, 104(10), 517–532. Klein, C. (2015a). What the body commands: The imperative theory of pain. MIT Press. Klein, C. (2015b). What pain asymbolia really shows. Mind, 124(494), 493–516. Klein, C. (2017). Pain, care, and the body: A response to de Vignemont. Australasian Journal of Philosophy, 95(3), 588–593. Langland-Hassan, P. (2017). The incorrigibility of pain. In The Routledge handbook of philosophy of pain, J. Corns (ed.). Taylor & Francis Group, 245–254. Livingston, W. (2012). Pain mechanisms: A physiologic interpretation of causalgia and its related states. Springer Science & Business Media. Loeser, J. D., & Volinn, E. (1991). Epidemiology of low back pain. Neurosurgery Clinics, 2(4), 713–718. Martínez, M. (2011). Imperative content and the painfulness of pain. Phenomenology and the Cognitive Sciences, 10(1), 67–90. Martínez, M. (2015). Pains as reasons. Philosophical Studies, 172(9), 2261–2274. McGinn, C. (1982). The character of mind. Oxford University Press. Melzack, R. (1975). The McGill pain questionnaire: Major properties and scoring methods. Pain, 1(3), 277–299. Melzack, R., & Wall, P. D. (1988). The challenge of pain. 2nd edition. Reprint, London: Penguin Books, 2008. Melzack, R., Wall, P. D., & Ty, T. C. (1982). Acute pain in an emergency clinic: Latency of onset and descriptor patterns related to different injuries. Pain, 14(1), 33–43. Nagasako, E. M., Oaklander, A. L., & Dworkin, R. H. (2003). Congenital insensitivity to pain: An update. Pain, 101(3), 213–219.

The Need for Complexity  83 Nikolajsen, L., & Christensen, K. F. (2015). Phantom limb pain. In Nerves and Nerve Injuries, 23–34. Academic Press. Osuntokun, B. O., Odeku, E. L., & Luzzato, L. (1968). Congenital pain asymbolia and auditory imperception. Journal of Neurology, Neurosurgery, and Psychiatry, 31(3), 291. Price, D. D. (2017). A view of pain based on sensations, meanings, and emotions. In Routledge handbook of philosophy of pain, J. Corns (ed.). Taylor & Francis Group, 113–223. Quine, W. V. (1960). Word and object. MIT Press. Reuter, K., & Sytsma, J. (2018). Unfelt pain. Synthese, 1–25. Rubins, J. L., & Friedman, E. D. (1948). Asymbolia for pain. Archives of Neurology & Psychiatry, 60(6), 554–573. Strigo, I. A., & Craig, A. D. (2017). A neurobiological view of pain as a homeostatic emotion. Routledge handbook of philosophy of pain, J. Corns (ed.). Taylor & Francis Group, 98–112. Sytsma, J., & Reuter, K. (2017). Experimental philosophy of pain. Journal of Indian Council of Philosophical Research, 34(3), 611–628. Tye, M. (2005). Another look at representationalism about pain. In Pain: New essays on its nature and the methodology of its study, M. Aydede (ed.). MIT Press, 99–120. de Vignemont, F. (2015). Pain and bodily care: Whose body matters? Australasian Journal of Philosophy, 93(3), 542–560. Weinstein, E. A., Kahn, R. L., & Slote, W. H. (1955). Withdrawal, inattention, and pain asymbolia. AMA Archives of Neurology & Psychiatry, 74(3), 235–248.

3

Mechanistic Explanations How Complex Idiosyncrasy Undermines Them

3.1 Introduction Pain is a posit of our everyday theory. It first began to be referenced by everyday people, going about their everyday lives, carrying out their everyday purposes. Pain is not, by contrast, a posit of one of our specialised theories—including one of our specialised, scientific theories. It was not discovered in the lab, like a protein. It’s not something, like dark matter, which we have posited to explain the explanatory or predictive success of other of our scientific theories. Rather, we began to reference pain as part of the common, everyday way that we make sense of ourselves and others. It is something which we are taught to identify in ourselves and others from a very young age. In my American upbringing, I began by using the words ‘owie’ or ‘boo-boo’ to refer to those things that hurt and felt nasty; those things for which I needed compassion and help; and those things which damaged me. Our belief in the existence of pains isn’t, accordingly, the result of any specialised, scientific theory, but is instead part of the everyday way that we have been taught to make sense of ourselves and our world during our everyday, humdrum interactions. Though pain is a posit of our everyday theory, we may nonetheless think it obvious that it is also something which science appropriately studies. One reason to think this is that whatever exactly pain is— whether it’s something mental or extra-mental—it surely has some important connection to our bodies. And our bodies, we might think it obvious, are appropriately subject to scientific study. Like hunger, we might think, pain is something we feel in our bodies that we can thus also deploy the scientific method to learn more about. Like vision, we might further think, pain is a way that we get information through our bodies which is also thus just as amenable to scientific investigation. In the modern light of evolutionary theory, we might also think it is just obvious that pain is something which has been naturally selected. It might initially seem obvious that pain is useful and helps us to survive. The short lives of those incapable of feeling pain may seem to provide further support for this idea (e.g. Nagasako et al., 2003). If pain has been naturally selected, then perhaps this alone renders it something about

Mechanistic Explanations  85 which science rightly offers generalisations. Finally, some of us might think that everything which exists is appropriately subject to scientific inquiry; if pain is real, then it’s appropriate for science to study it and offer generalisations about it. While I want to maintain, with our everyday theory, that pain is successfully and usefully referenced for everyday purposes, in this chapter and the next I will argue that pain is nonetheless not usefully referenced in scientific generalisations for explanation and prediction. Recall from Chapter 1 that we might call those kinds which are usefully referenced in scientific generalisations for explanation and prediction—natural kinds. A core claim of this book, then, is that pain is not a natural kind. Going further, we will be interested not only in references to pain as such, but to more particular types of pain. As I might have put it as a kid: certain kinds of owes and boo-boos. We can then divide the question of whether pain is a natural kind into two: first, whether pain, as such, is a natural kind, and second, whether any more particular type of pain is a natural kind. We might, that is, ask not only whether it is useful to refer to pain for scientific purposes, but whether it is useful for those purposes to refer to pain types. Settling the first question doesn’t settle the second. It may be useful to refer to particular types of pain—headaches, chronic pain, or cancer pain, say—even if it isn’t useful to refer to pain as such. For science, I’ll argue that references to both pain and pain types should go. At least, they should be eliminated from scientific generalisations. Not only is pain not a natural kind, no type of pain is a natural kind. References to pain lack scientific utility. We’ll begin to consider whether pain is usefully referenced for scientific explanation and prediction by looking, in this chapter, at whether there is a mechanism, or system, for pain or any pain type. Recall from Chapter 1 that the reasons to consider mechanisms when thinking about scientific utility include (1) that many think pain is usefully referenced in scientific inquiry, because they assume there is a pain mechanism, or system; (2) that many think that all natural kinds are mechanistically explicable; and (3) that many think that scientific inquiry about mental kinds of things, in particular, aims at mechanistic explanation. Further reason to consider whether there is a pain mechanism, or system, was revealed in Chapter 2, where we saw that the leading philosophical theories of pain, and the orthodoxy of simplicity with which they begin, may potentially be salvaged by identifying a pain system. Indeed, insofar as these theories depend on the functioning of a pain system to characterise pain or its posited content, as is most explicitly the case with psychofunctionalism, they may require that there is such a system. And, of course, the question of whether there is a mechanism for either pain or pain types is of interest in its own right. To avoid unnecessary complications, recall also that we are going to work with a very liberal idea of mechanisms, or systems—using

86  Mechanistic Explanations ‘mechanism’ and ‘system’ interchangeably for all present purposes. More specifically, we’ll take mechanisms, or systems, as wholes, with parts, that are organised and do things. We’ll take pain (or anything else, including pain types) to be mechanistically explicable if there is a whole, with parts, such that the organisation and goings-on of the parts determines, or explains, the pain. Though this leaves us with a very liberal notion of mechanism, or system, this is as it should be. We could have used more restrictive ideas of mechanisms or mechanistic explanations, but it would have then been even easier to show that there aren’t any for pain or pain types; by using such a liberal notion, we make the current task more difficult. Going liberal also allows us to avoid irrelevant debates concerning more restrictive ideas about mechanisms or mechanistic explanations. This way, we can conclude that even when we are liberal about what counts as a mechanism or mechanistic explanation, these are lacking for pain or pain types. In this chapter, we’ll focus first on mechanistic explanation for pain and then turn to pain types. For mechanistically explaining pain as such, we’ll consider the four neuroscientific models that have dominated pain research in the last 50 years. In Section 3.2, we’ll look at Melzack and Wall’s colossal gate-control theory, followed by a briefer overview of Donald Price’s somatic perception theory in Section 3.3, Craig’s homeostatic emotion theory in Section 3.4, and the pain neuromatrix theory in Section 3.5. I’ll argue that none of these identify a pain mechanism which can explain the wide range of tokens—that is, individual, particular instances—of the many types of pain. Indeed, as we’ll see, some of these theorists are explicit that they have not done so. The failure of these models to yield a mechanistic explanation for pain may, however, simply be thought to suggest the need for a better model. In response, we turn to what we already know about pain types. We’ll see in Section 3.6 that different types of pain implicate different mechanisms, such that we now know that some mechanisms are involved in some token pains and not in others. It is what we already know about the mechanisms implicated in pain types which allows us to conclude against any eventual mechanistic explanations of pain as such. An explanation of all pains as determined by some single pain mechanism, or system, is not forthcoming. In Section 3.7, going further, we’ll turn to mechanistic explanations of pain types. Recent work in pain science attempts to provide mechanism-based classifications and explanations of pain types, and the admitted failures thus far are instructive. What they are finding, in short, is that not only do different pain types involve distinct mechanisms, but that each token pain results from the convergent activation of multiple mechanisms—genetic, chemical, biological, social, and more. The central reason that no mechanistic explanation even for pain types is forthcoming is that the convergent activity of these multiple mechanisms is idiosyncratic. Idiosyncrasy is crucial for

Mechanistic Explanations  87 explaining pain tokens, but it blocks successful mechanistic explanations about pain types. It is what we already know about the mechanisms implicated in token pains which allows us to conclude against any eventual mechanistic explanations of pain types. I’ll conclude that neither pain nor any pain type will submit to mechanistic explanation. Though this conclusion apparently makes a prediction about the further deliverances of science, it is based firmly on pain science. It is pain science which, however surprisingly, has discovered that neither pains nor pain types are mechanistically explicable. Even if there is no mechanism for pain or pain types, we might still think that these are usefully referenced for scientific inquiry. After all, it might be objected, the useful scientific work that ‘pain’ is apparently being employed to do is evidenced by this very chapter! And, as per the liberal scientific utility criterion offered in Chapter 1, it’s utility that matters. While the lack of a mechanistic explanation may be a strong reason to think that a kind is not a natural kind, I’m not taking it to be decisive. In Chapter 4, accordingly, I’ll argue directly that the complex idiosyncrasy which undermines mechanistic explanation also undermines scientific utility. Token pains are highly idiosyncratic experiences which are not usefully generalised about for scientific inquiry. Science offers generalisations, but pains are the result of convergent processes whose convergence is too idiosyncratic to be usefully generalised about for any scientific purposes. Whether pains are nonetheless successfully and usefully referenced for everyday purposes is the question we’ll take up in Chapter 5.

3.2 Melzack and Wall’s Gate-Control Theory Does Melzack and Wall’s gate-control theory yield a mechanistic explanation of pain? Despite the influence and importance of the theory, and the important identification of the gate-control mechanism, I’ll argue in this section that there is no identification here of a whole, with parts, whose organisation and activities determine pain. Appreciating Melzack and Wall’s gate-control theory requires a few words on the history of pain science. One approach to that history is through the debates among pain scientists, and two of these are particularly relevant. The first is the traditional debate about what sort of thing pain is. A common way of presenting the debate within science is as of a competition between three main theories: the intensity theory, the sensory theory, and the affective theory. According to the intensity theory, pain is best understood as a perceptual experience, but one that can arise through any modality if the input is strong enough. An intense enough sound (e.g. very high-pitched), sight (e.g. very bright), or an

88  Mechanistic Explanations intense sensation of any other type will constitute a pain. By contrast, the sensory theory characterises pain as a distinct perceptual modality, subserved by a specialised system. On this view, even as audition and vision are distinct perceptual modalities, subserved by distinct receptors, pathways, and neural areas, so is pain a distinct perceptual modality, subserved by distinct receptors, pathways, and neural areas. The affective theory of pain classifies pain as a particular qualitative affect; pains are a particular unpleasant feeling. Traditionally, affective theories construed pains and pleasures as more akin to emotions like joy and sadness, than to perceptual modalities like audition. It is perhaps best understood as construing pain as the extreme end of a spectrum whose opposite end is pleasure. Competition among these three theories was fierce and is as old as Aristotle. Karl M. Dallenbach (1939, p. 337) describes the debate this way: The intensive theory and the sensory theory stood in opposition to one another, and they both stood in opposition to the traditional pleasure-pain theory which represented pain as an affective quale. In the decade between 1886–1896, these different opinions clashed and a three-cornered controversy ensued, the like of which has never before, nor since, appeared in the scientific literature. By the time he writes his history, Dallenbach takes the intensity theory to have been completely disproved, the affective theory to have been recast so as to no longer be a contender, and the sensory theory to be, if only partly established, well on its way to completion. He concluded, accordingly, that pain is a distinct perceptual modality. The evidence seemed to him incontrovertible that pain was subserved by dedicated, specialised fibres and that dedicated, specialised pain pathways were being discovered even as he wrote. It was just a matter of time, Dallenbach and most working scientists of the day thought, until the specialised pain mechanism, or system, was fully uncovered. The second line of debate concerns whether pain should be understood as a specific phenomenon or a convergence of many non-specific phenomena. In the sense at issue, a ‘specific’ phenomenon is one that is determined by activities in biological structures which are dedicated to that very phenomenon, whereas a ‘convergent’ phenomenon is determined by the convergence of activities in multiple structures, none of which are dedicated to its occurrence.1 Audition, for instance, is a paradigmatically specific phenomenon, whereas cognition is a paradigmatically convergent phenomenon. A.D. Craig’s (2003a) presentation of the history of pain science focusses on this debate. The issue is whether, as he puts it (p. 1), pain is a “distinct sensation represented by specialized elements both peripherally and centrally” or rather an

Mechanistic Explanations  89 “integrated, plastic state represented by a pattern of convergent somatosensory activity within a distributed network”. Species of the former view are specificity theories, whereas species of the latter are convergent theories. Before Melzack and Wall, the leading theories were all specificity and sensory theories. Is there a pain centre in the brain? Are there receptors just for pain? Are there pathways specialised for pain processing? Is pain a distinct modality? Is there a specialised pain system? The leading answers were all affirmative. To all of these questions, Melzack and Wall offered resounding negative answers that continue to reverberate. The central insight and influence of their gate-control theory (detailed further below) is the claim that the phenomenon which we call pain results from the activity of multiple, converging mechanisms, none of which are specific to pain. The shift from sensory, specificity theories to multidimensional convergence revolutionised pain science. As they (1988, X) put the point: The revolution began with a radical shift away from the traditional concept of a specific pain pathway to a brain centre where pain sensation is felt—a single sensory dimension that varies only in intensity. Instead, the gate-control theory postulates that pain is a unified stream of experience that is generated by the brain and is influenced by all of its cognitive functions such as memories of prior experiences and the meaning of the current situation. The spark that starts the fire is the denial that pain is a distinct modality; it is not subserved by specialised receptors, specialised pathways, or specialised cortical areas. Melzack and Wall straightforwardly deny that there is any such thing as a ‘pain centre’, for instance (1988, p. 122): “… the old concept of a ‘pain centre’ is obviously nonsense. Many areas of the brain are involved in pain processes and they interact extensively”. In denying sensory specificity, the gate-control theory instead characterises pain as an experience resulting from the wildly complex interaction of multiple systems. In sum (1988, p. 132): It is now becoming increasingly evident that virtually all of the brain plays a role in pain. Even seemingly unrelated brain activities such as seeing, hearing and thinking are important. Seeing the source of injury, hearing the sounds that accompany a rifle shot or a falling beam, and thinking about the consequences of an injury all contribute to the pain. Any satisfactory understanding of pain must include all of these processes which interact with inputs from the injured area or from deafferented neurons that produce pain signals when injury is absent.

90  Mechanistic Explanations This convergent model now dominates the field and has legitimised research into the effects of almost anything on pain—fostering new, previously unimaginable, treatments. What led Melzack and Wall to pioneer such a dramatic shift? Their theoretical starting point is the same mismatch between tissue damage and pain that proved fatal to the representational theories discussed in Chapter 2 (1988, p. 3): This is the essence of the puzzle of pain. Why are pain and injury not always related? What activities of the nervous system intervene between injury and pain perception that make the relationship so variable? Their theory was explicitly devised to explain not only pain caused by injury or tissue damage, but the many kinds of pains not caused by or involving any tissue damage. Further, they explicitly claimed that an adequate explanation of pain should explain not only why we sometimes have pain without tissue damage, but also why we sometimes have tissue damage without pain. Ultimately, the lack of correlation between pain and any distinct activity in the body led Melzack and Wall to claim that specificity theory, in any of its forms, was untenable. They reasoned persuasively, and influentially, that if pain were the result of specific receptors, pathways, and cortical centres, then surgical intervention or lesions of those receptors, pathways, and centres should abolish the pain. For any candidates: it did not. Rather than discard the ideas of their predecessors entirely, however, Melzack and Wall accepted that the mechanisms posited by specificity, sensory theories were indeed implicated in many token pain experiences (1988, p. 164): However, when all the theories—from specificity theory onward— are examined together … it is apparent that each successive theory makes an important contribution. Each provides an additional mechanism to explain some of the complex clinical syndromes or experimental data that were previously inexplicable. Previous theories should not be rejected—they should be supplemented. While inadequate to explain the wide range of pain phenomena, the theories are not strictly incorrect, but incomplete. The gate-control mechanism which gives the theory its name, likewise, is presented as a mechanism implicated in many token pains, and its postulation is motivated by the need to explain some token pains that no previous theories could explain. That the gate-control mechanism is one among many mechanisms which may contribute to the explanation of any particular pain is a point to which we return below. Let’s first take a closer look at the eponymous mechanism.

Mechanistic Explanations  91 In development since the 1960s, in the final presentation of the view (1988), the gate-control mechanism is presented as a five-stage pain mechanism. Below is a brief overview of each stage, including developments of the theory between its original and final presentations. Stage 1 is, in essence, specificity theory. Two types of small-diameter nerve fibres, Aα (myelinated) and C (unmyelinated), deliver impulses to the spinal cord when stimulated.2 These small-diameter fibres have high thresholds, i.e. they preferentially respond to relatively intense stimulation. Their high-intensity thresholds make these fibres the most likely candidates for pain-specific receptors or so-called nociceptors. Their input is received in the dorsal horn of the spinal cord by “transmission” cells, often simply called T-cells. These T-cells, in turn, transmit the received information to both local reflex circuits and on to the brain. As Melzack and Wall put it (1988, p. 166), “[t]his stage incorporates all that is shown in Descartes’ concept of pain”. All that is added to Descartes’ famous depiction of a version of specificity theory (Figure 3.1) are the T-cells in the spinal cord. Since gate-control theory’s inception, our knowledge concerning small-diameter fibres has advanced considerably. Of central relevance for our purposes is that the functionality of these fibres and their interactions is more complex than previously thought, such that the correlation between their stimulation and pain is even more variable than previously thought. By 1988, Melzack and Wall no longer thought that the small-diameter fibres (the so-called nociceptors) were usefully grouped

Figure 3.1 Descartes’ Pain Model.

92  Mechanistic Explanations as serving the same function, claiming instead (p. 171) that “… new data… show that myelinated [Aα] and unmyelinated [C] fibres have totally separate functions…”. A key difference is that C fibres become desensitised to repeated stimulation, i.e. it takes more and more intense stimulation to activate them, whereas Aα fibres become more sensitised, i.e. it takes less and less. This difference implicates different roles for C and Aα fibres in distinct pains—most obviously, their distinct roles in any prolonged pain or pains caused by repetitive injuries. Another relevant discovered difference is that these fibres do not terminate in the same place in the dorsal horn. The receiving T-cells were originally posited as being in the substantial gelatinosa (lamina I and II), but these transmission cells have themselves been somewhat discredited as a unified class. Melzack and Wall eventually conclude (p. 171) that “… there is not a hint of a simple, straight-through transmitting cell”. As discussed further below, the functionality of the T-cells in the gate-control mechanism makes mismatches between pain and either or both of Aα and C fibre firing to be expected. Increased understanding of the fibres only further confirmed these mismatches. Melzack and Wall deny that specificity theory, or stage 1 alone, can account for the now well-established mismatches between not only injury and pain, but activity in high-threshold receptors and pain. They write, for instance (p. 171): First, the onset of firing does not coincide with the onset of pain. Second, the time course of firing relates very poorly to the time course of pain. Third, identical pains evoked by different stimuli such as punctate pressure or heat are associated with strikingly different patterns of activity in afferent fibres. Specificity theorists carefully avoid discussing pathological pains, which, they admit, do not follow the rules of the normal nervous system. However, it seems totally unsatisfactory to explain ‘normal’ pain and leave the pains which matter, those of the suffering patients, for a later time and another explanation. Our conclusion from the experimental results as well as from patients’ reports, is that pain is the result of an analysis by the central nervous system of the entire situation at the time, taking into account the firing of nociceptors as well as other data at its disposal. Their conclusion by 1988 was that evidence for the variability between activity in transmission from high-threshold fibres (so-called nociceptors) and pain had only increased—more firmly hammering the nails in the specificity coffin. Stage 2 posits excitatory interneurons in the dorsal horn that facilitate transmission from the small-diameter fibres to the T-cells. Interneurons

Mechanistic Explanations  93 are, broadly, neurons which allow transmission between neurons of different types—we might think of them as connector neurons. Excitatory interneurons increase (‘excite’) the action potential of the neuron receiving the transmission, whereas inhibitory interneurons decrease (‘inhibit’) its action potential. Synapses are junctions between neurons where transmission occurs, and most every synaptic region in the central nervous contains both excitatory and inhibitory interneurons which modulate synaptic transmission. In this case, the posited interneurons facilitate transmission between the small-diameter fibres and T-cells. The interneurons posited in stage 2 are excitatory: they increase (‘excite’) the action potential of the T-cell in response to input from the small-diameter fibres. Positing these interneurons was needed to explain the protracted firing of the T-cells after only brief transmission from the small-diameter fibres. They were later found to also explain a related and robust phenomenon called wind-up: short, brief transmission from the small-diameter fibres at regular intervals results in increasingly exaggerated responses by the receiving T-cells. This often results in pain that is disproportional to the input from the small-diameter fibres—high-intensity pain from stimulation that’s not nearly as intense. Again, notice, we are going beyond specificity theory to account for the variability between activity in high-threshold fibres, i.e. nociceptors, and pain. Stage 3 posits further receptors: large-diameter Aβ fibres. Like Aα fibres, Aβ fibres are myelinated (indeed, highly myelinated), but unlike either C or Aβ fibres, Aα fibres are most preferentially responsive to low-threshold stimulation. If there is a unified class of nociceptors, these fibres are apparently not among them. Nonetheless, however, they transmit to the T-cells. It was initially thought that T-cells were nociceptive-specific (NS) cells, i.e., they could receive input only from high-threshold (small-diameter) fibres. Further investigation, however, revealed that this was not so. Instead, there are three kinds of T-cells in the dorsal horn: NS cells, wide-dynamic range (WDR) cells, and an unnamed group that respond only to low-threshold input. WDR cells can receive input from both high-threshold (small-diameter) and low-threshold (large-diameter) fibres. Melzack and Wall consider WDR cells to be “… by far the most common of the centrally projecting cells which signal injury”. It is worth emphasising that WDRs are both crucial for the gate-control mechanism and not specific to pain processing. This marks a major departure from specificity theory (1988, p. 167): The specificity theorists concentrated on the NS cells as the only cells that could be involved in triggering pain. We, on the other hand, simply proposed that pain would be triggered if the firing rate of any group of cells exceeded a critical level determined by the properties of the brain.

94  Mechanistic Explanations Note that whether or not the firing rate of the transmission cells in the dorsal horn reaches the “critical level” for pain is not determined by local mechanisms in the dorsal horn alone. As we’ll see below, this foreshadows the massive, and hitherto under-appreciated, contribution of the brain to whether incoming signals are processed in a way which, in a particular case, results in pain. Though there is now extensive confirmation of the dorsal horn’s three transmission cell types, controversy remains about which to emphasise in explaining pain. Some continue to emphasise the role of the NS cells, i.e. those which are only responsive to transmission from high-threshold receptors. Settling this controversy would take us too far afield. Melzack and Wall cite a number of studies that they think support their claim that (1988, p. 173) “…pain is related to the WDR cells rather than the NS cells…”. Important for our purposes is that WDRs are crucial for the gate-control theory, and it is currently the prospects of that theory for identifying a mechanism whose activities determine pain that we are considering in this section. Stage 4 posits gate-control theory’s most famous component: the inhibitory interneurons acting on transmissions from large-diameter fibres. Interneurons, remember, are connector neurons. Antecedent research revealed that T-cells were inhibited, i.e. their action potential decreased, when large-diameter fibres were stimulated. Inhibitory interneurons in the dorsal horn, receiving large-diameter impulses and modulating, i.e. inhibiting T-cell transmissions, were therefore posited. Notice that this means that fibres projecting to the T-cells can both excite (as discussed in stage 2 above) and inhibit T-cells: they have a “double effect”. The inhibition versus excitation of the T-cells plays a crucial role in determining whether the T-cells will, in turn, transmit the signal on to the brain—where, in turn, further activities may (or may not) occur such that pain is engendered. The phrase ‘gate-control’ is a metaphor for the T-cell levels of inhibition versus excitation: inhibition versus excitation levels of the T-cells determine whether the “gate” is “open”, and the transmission is passed on beyond the spinal cord’s dorsal horn, or whether the “gate” is instead “closed”, and the transmission is not passed any further. It was the recognition of the role of inhibition, above all, that gave the theory such explanatory power and led to novel treatment interventions. Treatments, especially for some tissue damage and injury-related pains, could be targeted at increasing inhibition and ‘closing the gate’. In their 1988 presentation, Melzack and Wall present numerous developments in dorsal horn inhibition research. Highlights include: •

Low-level electrical stimulation that preferentially activates largediameter receptors called TENS (for transcutaneous electrical nerve stimulation) is now used as a form of treatment. It is a method for

Mechanistic Explanations  95

•

•

“closing the gate”. As an everyday touchstone: consider rubbing your toe after stepping on a tack. Intense stimulation of small-diameter fibres is now thought to sometimes inhibit their otherwise excitatory effects on T-cells via an inhibitory mechanism involving the brainstem called DNIC (diffuse noxious inhibitory control). In short, one high-threshold transmission inhibits another by way of the brain stem. DNIC may explain what is sometimes called “counter-irritation”. As an everyday touchstone: consider pinching yourself in one place when you’ve been burned in another. T-cells were discovered to also be inhibited by endogenous opioids, i.e. the opioids your body internally produces. This led to treatment interventions involving micro-injections of exogenous opioids, i.e. opioids produced outside the body, into the dorsal horn. Morphine, in particular. As an everyday touchstone: consider cutting your finger while laughing or directly after exercise whilst your brain is flooded with ‘happy’ chemicals.

Notice that multiple explanations for variability between high-threshold stimulation and pain that are unavailable to the specificity theorist are already made available by stage 4 of gate-control theory. Recognising the crucial role of non-pain-specific components and activities, especially large-diameter fibres specialising in low-level threshold transmission, is important for explaining the variation between pain and the transmission of information about noxious stimulation. Thinking about the levels of inhibition versus excitation of the T-cells allows us to begin to understand why sometimes burns don’t cause any pain, why light touch sometimes causes intense pain, and why—in general—the correlation between pain and noxious stimulation (classed either as tissue damage, injury, potential damage, etc.) is so poor. There was, however, yet more variability still to be explained, leading to the final stage. The fifth stage of the gate-control mechanism posits downstream influence on the inhibitory neurons in the dorsal horn from the brain and includes a feedback loop from the spinal cord to the brain and back again to the inhibitory neurons. That the brain exerted some influence was known well before gate-control theory. The loop was originally posited on the assumption that ascending information affects descending modulation. Despite extensive research, however, the brain’s descending influence on the inhibitory neurons is still only poorly understood. The original model of the gate-control mechanism represented this downstream modulation by including an arrow to the dorsal horn from a box representing the brain called “central control” (see Figure 3.2). The theory brought new appreciation of just how central this downstream modulation was for whether there was pain on a particular occasion.

96  Mechanistic Explanations Though downstream modulation is still somewhat mysterious, there have been advances. As above, there was some initial evidence that the T-cells posited in the gate-control mechanism were subject, as Wall and Melzack (1988, p. 169) eventually put it, to “…powerful, steady inhibition [that] flowed continually from the brain stem”. More and more descending, inhibitory, modulatory pathways from brain to spinal cord and back again have since been discovered. Beyond the brain stem, it has become clear that the idea of a single path of descending control on some single type of T-cell is woefully over-simplified; many transmission cells are relevant to pain processing, and there are many paths of descending control modulating the activity of these cells. As in the introductory quotes above, Melzack and Wall held that almost the entire brain exerts not only inhibitory, but excitatory, control over local and ascending dorsal horn transmission. Even by 1988, however, all they think we have are (p. 176) “… very crude phenomena which can hardly explain the presence of an elaborate, interconnected, many-factored control mechanism”. They offer a crude approximation of a ‘subtle two-stage mechanism’ for descending control (p. 176): …1) the brain gives ‘permission’ to local circuits in the spinal cord to respond if the situation merits the response, and 2) the local spinal cord circuits measure the input and trigger a reflex response if they are permitted to do so by the brain, and if the afferent input is sufficient. This is obviously merely a mechanistic sketch that needs considerable filling in. Much contemporary work continues to focus on increasing our understanding of descending modulation (e.g. see Porreca, 2015 or White et al., 2018). In accordance with these five stages, the gate-control mechanism for pain presented in Melzack and Wall’s original paper was represented as per Figure 3.2.3 ‘S’ and ‘L’ represent large- and small-diameter fibres, ‘SG’ represents the substantia gelatinosa (lamina I and II), ‘T’ represents transmission cells, and ‘+’ and ‘−’ represent excitation and inhibition, respectively. Recall that a central inspiration for Melzack and Wall’s radical supplementation of the then-popular specificity theory was its failure to account, and so facilitate adequate treatment, for a wide range of pains. The inclusion of the complex interactions of non-specific components, by contrast, was explicitly included to facilitate new explanations of a wide range of pain phenomenon available—with the aim of illuminating novel treatment interventions. Recall also, however, that it was not only the dominant claim that pain was a specific phenomenon which Melzack and Wall revolutionary rejected but the related sensory theory of pain. Not only did the

Mechanistic Explanations  97

Figure 3.2 Gate-Control System.

gate-control mechanism include multiple components not specific to pain or high-threshold processing, but the inclusion of these components facilitated the rejection of sensory theories. In addition, then, to positing a specialised system with specialised components, a major failing of the predominant view of pain was that it recognised only pain’s sensory dimension. They write (1988, p. 161): The sensory approach to pain… valuable as it has been, fails to provide a complete picture of pain processes. The assumption that pain is a primary sensation has relegated motivational (and cognitive) processes to the role of ‘reactions to pain’…. It is apparent, however, that sensory, motivational and cognitive processes occur in parallel, interacting systems at the same time. … [These] processes must be included in any satisfactory theory of pain. Taking pain to be a purely sensory phenomenon was, they argued, insufficient. Melzack and Wall go on to lament that (1988, p. 191) “[t]he concept of pain as purely a sensory experience long overshadowed the affective and cognitive dimensions of the total pain experience”. These additional dimensions were taken by Melzack and Wall to receive introspective support: what people report it being like for them to be in pain, from the inside, is not limited to sensations in their bodies, but includes feelings, thoughts, evaluations, and motivations. As noted in previous chapters, my own introspection supports this multidimensional account of pain—and so, it seems to me, does our everyday theory of pain. Going

98  Mechanistic Explanations beyond introspection as reported using everyday theory, however, Melzack and Wall argue that the multiple, dissociating dimensions of pain are predicted by the multiple ascending pathways from the spinal cord implicated in pain processing that were discovered throughout the 1950s. Processing in these pathways occurs in parallel, in streams that interact with each other and other aspects of pain processing, and exerts influence on whether the gate is “open” or “closed”. The combination of introspective reports and discovered explanatory mechanisms led Melzack and Wall to conclude that it is illegitimate to characterise pains’ affective and cognitive components as mere reactions to pain instead of genuine components. Sensory, specificity theories of pain were thus taken to be insufficient on four related grounds: they failed to explain the wide range of pain phenomena; they were inconsistent with pain reports; they failed to explain the multiple dimensions of any token pain; and they could not accommodate the multiple non-specific components and (ascending and descending) pathways which are implicated in many pains. Despite explicitly and repeatedly rejecting the sensory theory, pain is often still referred to by Melzack and Wall as a perceptual experience. Care is here needed. Melzack and Wall do not here mean a perceptual experience as against an affective or cognitive experience. The ‘perceptual experience’ of pain is taken to have at least three components, only one of which is sensory: a sensory-discriminative component, an affectivemotivational component, and a cognitive-evaluative component. Of these three components they write (1988, p. 192): It is assumed that these three categories of activity interact with one another to provide perceptual information regarding the location, magnitude, and spatiotemporal properties of the noxious stimulus, motivational tendency toward escape or attack, and cognitive information based on analysis of multimodal information, past experience, and probability of outcome of different response strategies. All three forms of activity could then influence motor mechanisms responsible for the complex patterns of overt responses that characterize pain. It’s important to continue to emphasise that these components are explicitly identified not as mere causes or consequences of pain, but as genuine components. Phenomena previously considered by many in pain science to be merely casually connected to pain were argued to be among its proper parts. Accordingly, the final version of the gate-control theory is represented as in Figure 3.3.4 Note that the motor mechanisms there indicated are intended to extend (as per 1988, p. 193) to “… all of the brain areas that contribute to overt behavioural response patterns”. This is truly extensive. Melzack and Wall note (1988, p. 193) that the relevant motor mechanisms “extend throughout the whole of the central nervous

Mechanistic Explanations  99

Figure 3.3 Gate-Control  Theory.

system” and “must be at least as complex as … the input systems we have primarily dealt with”. In beginning to consider whether Melzack and Wall have here identified a pain mechanism, or system, whose workings explain pain, note that even as Melzack and Wall take the gate-control system to be well established, by 2008 they also claim that explaining the wide range of pain phenomena requires recognising at least two other independent mechanisms. They write (1988, p. 176, emphasis added): Each of the five stages that made up the gate-control mechanism has been supported by subsequent work. However, they are not sufficient to explain some of the basic facts about pain… Two completely different mechanisms were later discovered which have no relation to the gate-control …. These two distinct mechanisms are both mechanisms of prolonged pain: one impulse-triggered and one transport-controlled (or central). It’s useful to briefly consider both. The additional impulse-triggered mechanism was needed, most centrally, to explain inflammatory pain. Injury often results not only in immediate acute pain, but continued soreness, tenderness, and difficulty using the injured body parts. These are the ‘pains of recuperation’ which featured centrally in the imperative theory discussed in the previous chapter. Aα-fibres have slower conduction velocities than C-fibres, and as inflammatory pain develops later than acute pain, specificity theorists had posited that “slow pain” resulted from Aα-fibre input. Inflammatory pain, however, was found to crucially include transmissions from C-fibres. Further complexities arose because different types of tissue (joints, periarticular tissue, viscera muscle, deep fascia, and skin) show

100  Mechanistic Explanations decreased ability to produce this long-term effect. As an everyday touchstone: note the oddity in saying that any of your organs are aching. While Melzack and Wall originally thought that inflammatory pain could somehow be accounted for by gate-control despite these complications, it became clear to them that the explanatory mechanism would instead need to be centrally controlled. While much was still sketchy, some facts about the way in which C-fibres functioned differently depending on the different kinds of tissues they innervate was thought to point the way towards an explanation. Of central interest for present purposes is their concluding (1988, p. 180) at the time of writing that “[a] picture [was] beginning to emerge of a second system of transmission control in the dorsal horn…”. This mechanism, note again, is independent of the gate-control mechanism, and was taken by Melzack and Wall as being necessary to explain (at least) some inflammatory pains, which the gate-control mechanism could not explain. The additional transport-controlled mechanism was initially posited to explain yet other pains, especially some centrally maintained neuropathic pains. Neuropathic pains are, roughly, pains associated with damage to the nervous system—either peripherally or centrally. Melzack and Wall had recognised that the gate-control mechanism could not explain at least some of these pains. Instead, they posited an independent mechanism which involved the transportation of chemicals in sensory fibres, with C-fibres being thought to play a particularly central role in transporting the relevant chemicals. Exactly what the relevant chemicals may be, however, was explicitly admitted to be unknown. The central point for present purposes is again that the functioning of this hypothesised mechanism of chemical transportation was taken to be independent of the functioning of the gate-control mechanism—hypothesised again, crucially, to explain pains which the gate-control mechanism could not explain. Despite any claims made by their disciples, Melzack and Wall are clear that though they think that they have identified a mechanism implicated in many pain experiences, they have not identified the pain mechanism whose workings explain all pain. This is not surprising. The claim that there is a single pain mechanism is antithetical to the spirit of their quarrel with specificity theory; they reject that there is a single mechanism specific for pain, and that any of the mechanisms implicated in pain have components specific for pain processing. Throughout their work they deny that there are any receptors, cells, pathways, or cortical centres that are appropriately understood as pain receptors, pain cells, pain pathways, or pain centres. For one example of a passage explicitly and characteristically antagonistic to such ideas, consider (1988, p. 157): …central cells that respond exclusively or maximally to noxious stimuli are not ‘pain cells.’ There is no evidence to suggest that they are more important for pain perception and response than all the

Mechanistic Explanations  101 remaining somaesthetic cells that signal characteristic firing patterns about multiple properties of the stimulus, including noxious intensity. The view that only the cells that respond exclusively to noxious stimuli subserve pain and that the outputs of all other cells are no more than background noise is purely a psychological assumption and has no physiological basis. Melzack and Wall take themselves to have identified a mechanism implicated in many pain experiences. That is certain. Their denial that it has components specific to pain processing is also certain, as is their detail that they have identified the pain mechanism whose workings explain all pain.5 3.2.1 At Least Two Worries about the Above May Be Raised First, even if there are pains which are not explained by the gate-control mechanism, we might take it to explain yet others. We might, that is, think the gate-control mechanism explains a type of pain that we might call gate-control pain. Against this proposal, notice first that the gate-control mechanism is represented as only one system among many in the schematic for pain presented in Figure 3.3. This begins to suggest that even those pains in which activities in the gate-control mechanism are implicated are not adequately explained by activities in the gatecontrol mechanism alone. We’ll return to mechanistic explanation for pain types in Section 3.7. For now, we are focussed on pain as such, and the discussion above hopefully makes clear that the gate-control mechanism fails to adequately explain pain as such; explaining pain requires, at least, appealing to additional mechanisms and systems, and many pains remain entirely unexplained by activities in this mechanism. The gate-control mechanism is not the pain mechanism. Second, however, while the gate-control mechanism may be only one among many whose activities contribute to explaining pain, we may take the schematic in Figure 3.3 itself to be an identification of the pain mechanism. We may, that is, take that schematic as identifying some overall whole, whose systems (including the gate-control mechanism) are themselves parts, and whose organisation and activities explain pain. Against this suggestion, I make three points. First, the previous point about the gate-control mechanism can again be made concerning each of the systems represented in the schematic. There are, that is, not only some pains for which the gate-control mechanism plays no role but some pains for which any combination of schematised systems plays no role. Abolition of any of these identified systems does not abolish pain, and, for each identified system, there are some pains in which activity in that system plays no explanatory role. This suggests that we do better to take the schematic as identifying many mechanisms, any of which may or may not be implicated in a token pain,

102  Mechanistic Explanations as against a unified whole—the pain mechanism—whose workings adequately explain pain. Second, the schematic is far too schematic for us to conclude that we have an adequate explanation for even any token pain, much less all pains. Consider, for instance, the box labelled ‘central control processes’. As described above, this box is included for two main reasons: the role of the brain in modulating dorsal horn transmission and centrally maintained pains. But we continue to lack any clear mechanistic understanding of the workings of either. There is little more to the role of this mechanism, as sketched in Figure 3.3, then the brain does some stuff. This is not adequate for explanation or prediction. And this inadequacy is evident from consideration of only this one box. The workings and interactions between other schematised systems are likewise, well, schematic. Were we to take gate-control theory as identifying the mechanism for pain, it is not clear the mechanism would be any more specific than, e.g., pain is determined by the workings of the brain and the body. This may be true, but it is not yet an adequate mechanistic explanation for pain: it does not tell us which parts are organised and do thing such that their organisation and goings-on determines pain.6 Third and finally, taking the gate-control theory to identify the pain mechanism, or system, is antithetical to Melzack and Wall’s own interpretation of their theory. In addition to their explicit and repeated rejection of specificity and sensory theories, they repeatedly and explicitly deny that pain is any single type of experience; for example (1988, p. 156), “… the term ‘pain’ is a broad label for countless different experiences”. They argue that the diversity defies definition (1988, p. 46): The diversity of pain experiences explains why it has been impossible, so far, to achieve a satisfactory definition of pain. The word ‘pain’ represents a category of experiences, signifying a multitude of different, unique experiences having different causes, and characterized by different qualities varying along a number of sensory, affective and evaluative dimensions. At present, we must be content with guidelines toward a definition rather than a definition itself. Too much remains to be learned about pain mechanisms before we can define pain with precision. Though they here imply that they think we are headed towards a definition, Melzack and Wall’s gate-control theory should nonetheless not be understood as providing one.7 According to the theory’s authors, pains are a category (an everyday posit, I’ve been stressing) of a motley set of unique and varied experiences, and these are not all mechanistically explained by either the gate-control mechanism or their overall sketchy schematic whose components include systems like the brain.

Mechanistic Explanations  103 Of course, Melzack and Wall may well have been wrong about their work. They may be wrong about either how unique and varied pains are, or—crucially—wrong about how explanatory their schematic in Figure 3.3 is. But I don’t think so. Despite failing to provide a definition of pain or to identify a mechanism which explains it, the gate-control theory revolutionised pain science. How? Putting the above points together allows us to see that the extensive influence of the theory can be understood less as a result of its specification of what pain is or what mechanistic activity explains it, than of what it can include. Its influence is not a result of identifying the pain mechanism, but instead of identifying multiple mechanisms any of which may, or may not, be implicated in a particular pain. Remember that immediately prior to the introduction of their theory, pain was taken to be exclusively determined by specialised receptors, spinal cells, pathways, and brain centres. Pain science and the diagnostics it spawned were thus vested in a straitjacket that left numerous sufferers without relief: those who did not respond to standard treatments targeted at “the pain mechanism”—a specialised, sensory system—were often thus considered to be malingering, confused, or mentally ill. Though many pains are regrettably still dismissed or ignored when failing to correspond to an overly simplistic model favoured by a particular clinician, in the wake of gate-control theory, things have nonetheless begun to change. For sufferers: the changes are for the better. Pains are now recognised to vary considerably, and it is recognised that a wide range of non-specific activities may determine whether a particular person undergoes pain on a particular occasion. Melzack and Wall identified a range of mechanisms—independently functioning mechanisms—whose workings may, on distinct occasions, explain distinct pains. The gate-control mechanism was one such particuarly influential and fruitful identication. As they write (1988, p. 273): The gate-control theory of pain has provided, in large part, the conceptual background—the foundation—for new approaches to pain. The theory argues that pain does not have a single cause and is not even a single entity. There are multiple, interacting physiological and psychological mechanisms, and a rational approach to pain control requires multiple approaches that converge to produce a reduction in pain. Including numerous, independently functioning mechanisms as implicated in distinct pains on distinct occasions has advanced our understanding of pain’s unique, varied, and multidimensional nature. And, crucially, has thereby improved treatment. The many new treatments are a testament to the better justice this complex account of pain does to the phenomenon than any of its predecessors. Yet again: for pain, treatment is the crucible for theory.

104  Mechanistic Explanations Gate-control theory revolutionised pain science by releasing it from the dogmatic grip of overly simplistic, sensory, specificity theories. In doing so, novel mechanisms which may be implicated on distinct occasions have been revealed as potential treatment targets. None of this, however, involves identifying a mechanism, or system, whose workings explain pain. Despite its undeniable importance, gate-control theory does no such thing.

3.3 Price’s Somatic Perception Theory Donald Price’s (1999) somatic perception theory of pain is heavily influenced by gate-control theory; indeed, ‘somatic perception theory’ is my own label for Price’s account, which may as well be understood simply as supplementing gate-control theory. It is nonetheless worthy of a brief, separate discussion, as it allows us to see the addition of yet further mechanistic activities, not specific to pain, which are sometimes implicated in distinct pain experiences. As is standard, Price followed Melzack and Wall in holding that pain has multiple components—sensory, affective, and cognitive—but went beyond them in appealing to these components, and a further associated feeling of threat, to offer a definition of pain. He writes (1999, p. 2): The definition I propose [of pain] is a somatic perception containing (1) a bodily sensation with qualities like those reported during tissue-damaging stimulation, (2) an experienced threat associated with this sensation, and (3) a feeling of unpleasantness or other negative emotion based on this experienced threat.8 Price explicitly claims (1999, p. 8) that these elements are individually necessary and jointly sufficient for pain, i.e. each of them is necessary for something to be a pain, and that only all three together will constitute a pain. The relevant sensation is held to arise via a distinct sub-modality of somatosensation. The somatosensory system, very broadly, processes information about the body including pressure, position, vibration, movement, and so on. Somatosensations are the perceptions this system yields including, accordingly, sensations of touch, bodily position, and so on. Price’s suggestion is that the sensory component of pain is a distinct type of somatosensation—there is a distinct qualitative character to pain, resulting from a subset of the activities of the somatosensory system. On Price’s view, this distinct type of somatosensation inherently disposes one to experience the further feelings of threat and unpleasantness that Price takes also to be necessary for pain. Central to our purposes is Price’s further claim, not explicit in the definition quoted above, that the sensation and associated experienced

Mechanistic Explanations  105 threat are taken to be modulated by the cognitive component of pain. In particular, they are modulated by the meaning that each particular individual attaches to the sensation and the threat itself. If I am a professional piano player, for instance, the breaking of my fingers will have a significance, or meaning, for me which alters the sensation and associated threat. Crucially, on Price’s view, cognitive evaluation of these is itself a component of pain. My particular evaluation is part of my pain; the significance of the threat and sensation that I am experiencing is not merely a reaction to the experience, it is part of the experience itself. And, as above, the unpleasantness of the experience is, in turn, based on the sensation and experienced threat. In this way, the cognitive evaluation also indirectly alters the unpleasant affect of the experience. To return to the above example, if I am a professional piano player, then the significance of the sensation and experienced threat involved in the pain of breaking my fingers is likely to cause the unpleasantness to be greater than it would be for many others who would differently evaluate the sensation and threat. The previous chapters’ discussions of our everyday theory of pain and some of the clinical evidence may give us reason to be sceptical of some of Price’s claims. The supposedly distinct sub-modality of somatosensation which he posits is highly controversial. Other subtypes of somatosensation like mechanosensation—sensations concerning changes in pressure or movement—or thermosensation—sensations concerning changes in temperature—have dedicated receptors and distinct qualitative characters. But we’ve now seen reasons to doubt that there are dedicated receptors for pain; the so-called nociceptors, which are preferentially responsive to high-threshold stimulation, are preferentially responsive to high-threshold stimulations from these other subtypes of somatosensation, e.g. high-threshold temperature or high-threshold pressure. Going yet further, as we’ve seen above, activity in these high-threshold receptors is neither necessary nor sufficient for pain. In the previous chapter, we’ve also considered some reasons to be sceptical that there is a distinct qualitative way that all pains feel, the pain quality—at least, once this qualitative character is carefully distinguished from sensory and affective qualities. We have, moreover, considered cases that are apparently pain, but which apparently lack any particular sensory or affective qualities. While I think these are good reasons to be sceptical of some of Price’s claims, we are not here centrally interested in whether or not we should accept Price’s definition of pain. Instead, we are here considering whether Price’s somatic perception theory, even if granted, yields a mechanistic explanation for pain. It does not. Though Price claims that pains have a distinctive qualitative character, far from harkening a return to specify theory and positing a

106  Mechanistic Explanations specialised pain system, Price’s model involves multiple, dissociating components and activities which are not specific to pain.9 As with gate-control theory, multiple descending pathways are here embraced as necessary to explain pain’s multiple dimensions. As the cognitive component of pain is emphasised by Price as modulating the other components, these descending pathways take centre stage. The information being processed is not merely sensory information; as above, it’s information concerning an individual’s particular cognitive evaluation of occurrent sensations and experienced threat. In addition, however, more than any of his predecessors, Price emphasises the multiple ascending pathways implicated in pain processing. His theory was influential largely for emphasising these ascending pathways and arguing that they are clues to understanding pain. And none of these pathways, note again, are specific for pain. The overall picture of multiple ascending and descending pathways that emerges is represented in the following oft-presented schematic10:

Figure 3.4 Price’s Pain Pathways. (From Price, 2000). (Key: ACC, Anterior cingulate cortex; Amyg, Amygdala; BG, basal ganglia; HT, hypothalamus; M1, primary motor cortex; PAG, periaqueductal grey, PB, parabrachial nucleus of the dorsolateral pons; PCC, posterior cingulate cortex; PF, prefrontal cortex; PPC, posterior parietal cortex; S1 and S2, first and second somatosensory cortical areas; SMA, supplementary motor area.)

Mechanistic Explanations  107 These pathways are all posited to contribute to explaining the sensory, affective, and cognitive dimensions of pain and their interactions. Price claims that each of these dimensions can be selectively influenced and, therefore, that assessing pain requires assessing each dimension (e.g. 1999, p. 69). Price makes explicit (1999, p. 211) that discovering distinct mechanisms that explain the distinct dimensions of pains is an ‘ultimate goal’ of pain science. To achieve this goal, pain scientists are exhorted to combine phenomenological reflection—people offering reports about their experiences from the first-person, i.e. from ‘inside’—with more mainstream third-personal methods. Phenomenological reflection is held by Price to be crucial, since, in addition to holding that all three conditions discussed above are necessary for pain, he holds that pains are necessarily conscious experiences.11 Notice that whatever process explains the consciousness of the pain is not included in the above schematic. It would, presumably, include yet further components, activities, and organisation. For our purposes, we can anyway set this claim about consciousness aside. More central is that Price claims that each dimension of pain must be separately subject to these third- and first-personal methods to identify their distinct mechanistic explanations. Like Melzack and Wall, Price explicitly and repeatedly (e.g. pp. ix or 99) claims that explanation of the multiple dimensions of pain requires identification of multiple mechanisms. Might we take the multiple mechanisms which may eventually be identified to explain the multiple dimensions of pain to constitute one overall pain mechanism whose workings explain pain? A whole, with parts, that are organised and do things such that their goings-on determine pain? As with gate-control theory, I think not. Figure 3.4 does not offer a mechanistic sketch of a unified pain system. As with gatecontrol theory: some of the composite mechanisms would be implicated in some pain experiences and not others, and the composite mechanisms themselves are currently only sketched, offering nothing like an adequate identification of the parts whose organisation and activities may be taken to constitute a whole which explains pain. Price himself certainly never insinuates that he has identified any such thing, and it is difficult to see why we should take him as so doing. The schematic identifies pathways which may be implicated in a particular pain. It does not identify anything appropriately dubbed the pain system. Setting aside the accuracy of Price’s model, or the status of many of his claims about pain’s nature, the relevant moral of the story is that Price’s somatic perception theory does not identify a mechanism that explains pain. His definition of pain includes multiple components, and he takes an ultimate aim of pain science to be an explanation of each of these dimensions through the identification of multiple mechanisms. These multiple mechanisms are posited as operating both in serial and

108  Mechanistic Explanations in parallel and differently contributing to different pains on different occasions. Price illuminatingly identifies a plethora of multiple ascending and descending pathways, any of which may or may not be involved in any particular pain. But there is no identification of a pain system, or mechanism, whose workings explain pain.

3.4 Craig’s Homeostatic Emotion Theory Though not advocating a full return to specificity theory, Craig’s theory of pain as a homeostatic emotion explicitly aimed to temper leading convergent views of pain, such as the somatic perception and gate-control theories above discussed. In particular, he alternatively emphasises the specialisation of a specific pathway implicated in pain experiences: the lamina I spino-thalamo-cortical pathway. Notice from the outset, however, that even on Craig’s view this pathway is not specific to pain—it is, instead, specific to homeostasis. Homeostasis is the body’s internal regulation to maintain equilibrium. Other homeostatic functions identified by Craig as being subserved by this pathway include hunger, thirst, and itch. Craig’s offered schematics of the homeostatic system, and its specialised pathway, include no labelling of any pain-specific components or patterns of activity. Here is one such characteristic image12 (Figure 3.5): On Craig’s model, input from small-diameter fibres (not depicted) terminates in the dorsal-horn’s lamina I. We have already seen this projection in the models in the previous sections, though projections from large-diameter fibres or projections to a range of T-cell types in not only lamina 1 but also lamina 2 are here absent. In explicit departure from other models, Craig represents small-diameter fibre inputs as being transmitted to the brain specifically through the lateral spinothalamic tract, as against the parallel, ascending processing streams, e.g. as depicted in Price’s model. Though Craig’s model includes only a single, specialised stream transmitting pain-relevant information to the brain, note that distinct termination locations of the identified projections are posited as explaining the sensory and motivational dimensions of pain: both of which are accepted by Craig as genuine, and distinct, components of pain. In particular, the interoceptive cortex is taken to subserve pain’s sensory dimension, and the distinct motivational dimension is taken to be represented in the anterior cingulate cortex (ACC). On Craig’s view, the homeostatic emotions are those which are comprised of these sensory and motivational components—both together. And again, these include not only pain, but itch, hunger, and thirst. Excepting their inputs, the model is taken to equally depict all such homeostatic emotions. Explaining homeostatic emotions, however, is not quite as simple as the schematic may be thought to imply. Craig holds that undergoing any

Mechanistic Explanations  109

Figure 3.5 Craig’s Homeostatic Model.

homeostatic emotion, including pain, requires that information from the privileged pathway be integrated with other streams of information in the forebrain (see, e.g., 2003a). This integration is not depicted above. Integration makes sense if homeostatic emotions are to fulfil their posited function of bringing the body into equilibrium. Information about the state of one’s tissues must be coordinated with information about, for example, the position of one’s limbs, if one is to perform an equilibrium-aimed action using those limbs. Going further, however, we are not taken by Craig to be having a homeostatic emotion at all, until the forebrain integrates this information. Thus, does Craig sometimes refer to homeostatic emotions as integrated perceptions. When we have an itch, for example, we have the itch somewhere, and having it there is part of having the itch. The necessity of integration of this non-specific information is the first glimpse that specificity theory is ultimately still rejected by Craig: to explain pain, understood as a homeostatic emotion,

110  Mechanistic Explanations requires the postulation of activity in components not specific for pain, or even specific for homeostasis. Further complexities arise if we seek to explain subjective, firstpersonal awareness of pain, i.e. the experience of pain. For this awareness, Craig holds that representations in the insular cortex must receive meta-representation in the anterior insula (see, e.g., 2003a, p. 24). These meta-representations are also not depicted in the above schematic. One may hold that pains sometimes occur without our being aware of them, i.e. perhaps some of our pains are not experienced. This possibility, however, is not one that Craig is willing to accept, holding instead that a mental episode is not a pain unless we are aware of it and that awareness of it requires a meta-representation.13 For Craig’s model, then, a full schematic must further include these meta-representations. Craig’s model thus follows specificity theory by emphasising specialised pathways (for homeostasis though, note again) and follows convergent theories by emphasising the integration of information from the activity in multiple non-specific (that is, not specific for homeostasis) mechanisms. Craig therefore rightly takes himself to be offering a middle way between specificity and convergence. He writes (2003a, p. 23): The neural substrates underlying pain sensation in this model include both specific sensory channels (virtual ‘labeled lines’) from lamina I and the convergent intensity-related pathways from lamina V. Integration of these multiple ascending pathways in the brainstem and the forebrain is necessary for homeostatic control, for integrated perception, and for behavioral arousal. The essential conceptual difference between the prior convergent model and the more specific view described … stems from the fundamental recognition that the various feelings from the body represented in the STT [spinothalamic tract] are all aspects of the sense of the body’s physiological condition, referred to as interoception, whereas the lemniscal fine touch and positional sense provide information about the relationship between the body and the external environment, that is, exteroception and proprioception. Rather than contrasting specificity and convergence, and pinning his flag to either, Craig advocates contrasting interoception and exteroception, and he pins his flag to the former. Recall from Chapter 2 that exteroception includes, roughly, perceptions of things external to the body, whereas interoception includes, roughly, perception of the internal states of the body. Craig laments the emphasis which other pain theorists have placed on WDR cells that patently subserve exteroception. Instead, he emphasises NS cells and a distinct class of cells posited by Craig called HPC cells (for heat, pinch, and cold, respectively),

Mechanistic Explanations  111 which he holds to instead subserve interoception.14 I emphasise that HPC cells, as posited, are responsive to much more than just noxious stimulation. Craig also laments that the crucial role of the insular cortex in homeostasis is under-emphasised in the dominant convergent theories of pain. It is, he argues, the specialised nature of both the lamina I cells and the insular cortex which allow the body to track the status of its internal state at all times. I emphasise that the body is thus held to be constantly tracking its internal states, not only when these are damaged or threatened. These specialised components are part of a hierarchical system in the body that subserves all homeostasis. Craig’s central problem with other convergent theories is thus not that they fail to recognise a pain-specific system, but rather that they inappropriately blur the lines between interoception and exteroception, thereby leaving us unable to appropriately identify the workings of a specialised homeostatic system. None of the emphasis on interoception as against exteroception is to deny his earlier claims that any homeostatic emotion, including pain, requires integration of information from multiple systems, or that awareness of the emotion (necessary for at least pain) requires a meta-representation. Accordingly, he summarily writes (2003a, p. 24): …the neural representation of pain involves both specificity and integration. Pain as a homeostatic emotion is, in humans, both a specific interoceptive sensation and an integrated affective behavioral drive caused by a physiological imbalance that automatic (subconscious) homeostatic systems alone cannot rectify. In explicitly going against alternative and dominant models of pain, it is unsurprising that Craig’s homeostatic theory is controversial within the pain science community. Reasons to doubt Craig’s theory may be extracted from the development of those already discussed. Craig’s model limits ascending pathways to the spinothalamic tract, whereas many have been impressed by the evidence offered in favour of including parallel ascending pathways—as depicted, for instance, in Price’s model. The privileging of the spinothalamic tract is thus questionable. Similarly, as we’ve seen, the inclusion of many of Melzack and Walls’s additional components and processing streams was explicitly motivated by the wide range of pains held to be unexplained without them. Insofar as Craig’s model is missing these, one might worry that many pains are inappropriately excluded from even the possibility of explanation using this model. Moreover and perhaps most centrally, one might doubt Craig’s core claim that pain—like itch, hunger, and thirst—serves a homeostatic function. This claim concerning the function of pain is the central reason which guides Craig to limit the components and activities included in his pain modelling. But, partly

112  Mechanistic Explanations based on the evidence of the many distinct components and pathways implicated in distinct pain experiences, one may reason in the opposite direction and reject this core claim. In particular, one may think that even if some pains, on some occasions, serve a homeostatic function, some pains do not, and many pains serve further biological functions. As Price (2017, p. 122) writes: This [Price’s own] view of pain as serving both exteroceptive and interoceptive functions and as having sensory and affective dimensions contrasts with views of pain as serving only a single function or dimension or even those that propose only one or two major pathways for pain… In the light of gate-control theory, the idea that pain serves both exteroceptive and interoceptive functions, and that there are multiple ascending pathways and integrated components which reflect these other functions, has become the majority view. If this majority view is correct, then Craig’s model is overly simplistic. As with the two theories above considered, however, we are not here centrally interested in whether we should accept Craig’s homeostatic emotion theory; instead, we are here considering whether, if granted, the theory yields a mechanistic explanation for pain. And yet again, I argue that it does not. In aiming to temper convergent accounts of pain, and identify more specific and specialised components and activities, Craig’s theory—if granted—may initially appear a promising candidate for having identified a mechanism whose workings explain pain. In particular, the theory apparently focusses on a distinct system. As noted, however, and as I now stress, the posited system is a homeostatic system. To identify this system, however, is not yet to identify a pain system. Neither the above model nor any commentary on the model clarifies when the homeostatic system results in pain as against any other homeostatic emotion. Indeed, as far as I can tell, Craig does not attempt to provide a mechanistic explanation for pain, in particular, as against other supposed homeostatic emotions, in any of his work. Indeed, expecting Craig to identify a pain mechanism, or system, is perhaps simply inappropriate. While Craig does aim to temper convergent theories of pain, he nonetheless explicitly follows them in rejecting the idea that pain is explained by the workings of a specialised system. Considering any subset of the components of the identified system won’t allow us to identify pain, i.e. the receptors, the pathways, or the relevant cortical structures. None of these are pain-specific. He explicitly denies, for instance, that ‘nociceptor’ and ‘nociception’ are anything but heuristics (2003a), emphasising that small-diameter afferents and their

Mechanistic Explanations  113 receiving transmission cells not only process information about noxious stimuli but are continually relating information about the body’s status. His own posited HPC cells would seem to tell against specialised components for pain. Craig’s claim is that the same components of the mechanisms are implicated when tissues are being damaged and when everything is just fine. If focussing on the components of the homeostatic system will not allow us to explain pain in particular, perhaps greater success will be garnered by appealing to the activities of the system. Again, however, no such activities are identified. Merely appealing to the workings of the system which constantly monitors the body’s internal states won’t suffice for determining or explaining when an agent is undergoing pain, which comes and goes. To successfully explain or predict pain (as ever: for treatment above all), we need to be able to determine which activities, if any, constitute pain. Nothing in Craig’s work allows us to do this. The moral is that while Craig may well take pain to be determined by some activities or other in the posited homeostatic system, we are not provided with any explanation of when or how. Absent this, we remain without a mechanistic explanation for pain. Notice finally that not only does Craig not identify components or activities in the homeostatic system which may explain or determine pain, he does not neatly distinguish between pain from any other homeostatic emotion. The nearest he comes, that I can find, is the following passage (2003b, p. 304, emphasis added): The basic homeostatic ‘feelings’ or modalities include temperature, itch, visceral distension, muscle ache, hunger thirst, ‘air hunger’ and sensual touch. All of these inherently generate an emotion that drives homeostatic behavior, and pain is no different. Pain normally originates from a physiological condition in the body that automatic (subconscious) homeostatic systems alone cannot rectify, and it comprises a sensation and a behavioral drive with reflexive autonomic adjustments. Pain can be either unpleasant (as usual) or pleasant (as when it relieves an intense itch). The behavioral drive that we call pain usually matches the intensity of the sensory input but it can vary under different conditions, and can become intolerable or, alternatively, disappear, just as hunger or thirst. Though much of pain is here predicated, there is not nearly enough to distinguish it from any other homeostatic emotion. It is, in fact, not clear to me that Craig thinks that pain is neatly distinguished from other homeostatic emotions. The only hint of distinguishing pain from other homeostatic conditions here is its origination conditions: ‘a physiological condition of the body’. But, as we’ve seen many times now, this

114  Mechanistic Explanations is hopeless for distinguishing pain. And Craig, as he repeatedly makes explicit, does not think that pain is constituted by the perception of any particular kind of damage or disturbance to the body. Going further, in speaking of “[t]he behavioral drive that we call pain” we might even think that just as Craig thinks ‘nociception’ and ‘nociceptors’ are simply heuristics, so too is ‘pain’. This interpretation may be further suggested by recent collaborative work (Strigo & Craig, 2017). In discussing thermosensation as a homeostatic emotion, for instance, the picture is apparently one of a distinct sensory type, i.e. thermosensation, with ‘an obligatory hedonic affect’. The authors write that combinations of sensation and affect, on some occasions depending on the body’s needs, ‘would be called painful’. A distinct mechanism for homeostasis is identified, and one too for thermosensation, but pain is merely what we call some combinations of activities in these systems on some occasions— combinations which remain without specification or mechanistic explanation.15 Though the philosophical imperativists sometimes appeal to Craig’s work (e.g. Klein, 2015, pp. 32–33 or p. 129), he himself gives no hint that pains are constituted by a distinctive (homeostatic) command—nor, again, does he seek to identify any particular components or activities which may subserve the giving of any such command.16 In closing this section, I want to make clear that I do not think Craig has aimed to identify a mechanistic explanation for pain and failed; rather, I think a better interpretation of Craig is to take him as offering something else entirely. Craig’s efforts have been focussed on convincing the pain science community that pain—along with a range of other affective bodily feelings—has a homeostatic function, to be explained by the workings of the homeostatic system. Identifying a pain mechanism was never the goal. Indeed, even explaining how the workings of the homeostatic system yield pain, as against any other homeostatic emotion, has not been on the agenda. Whatever his aims, the central result for present purposes is the same: Craig’s homeostatic emotion theory of pain—even if granted—does not yield a mechanistic explanation for pain. It may, at best, allow us to explain homeostasis. Even were it granted that some activities or other, of some components or other, organised some way or other, in the identified homeostatic system explain or determine pain, Craig does not identify what any of these ways are. A mechanistic explanation of pain cannot be extracted from Craig’s work—however impressive it may otherwise be. Going further and despite his tempering of convergent theories, it seems to me that his theory may—if anything—support rejecting the very search for a pain system, as against the homeostatic system. Whether or not this further point is granted, accepting Craig’s controversial model does not yield an identification of a pain system, or mechanism, whose workings explain pain.

Mechanistic Explanations  115

3.5 The Neuromatrix Theory of Pain The initial presentation of the neuromatrix theory can be traced to a lecture by Melzack (1989) in a discussion of phantom limb pain. Melzack explicitly posited the neuromatrix to explain pains that his earlier gate-control theory could not explain (phantom limb and chronic pain, in particular). The neuromatrix was there presented as a body-self neuromatrix: it is a model of the unified perception of the states of one’s entire body. It was intended to explain all experiences of the body. As originally summarised (1989, p. 1): “The neuromatrix imparts a pattern on all inputs from the body, so that experiences of one’s own body have a quality of self and are imbued with affective tone and cognitive meaning”. Pain was offered as one among many such experiences. Work on Melzack’s body-self neuromatrix hummed along in the background of pain research since its introduction, and it has increasingly come to the fore. In this section, we’ll briefly consider the neuromatrix theory, first as it was offered by Melzack, and then as it is discussed today. As with the theories above, we’ll ask whether the theory, even if granted, yields a mechanistic explanation for pain. As with the theories above, I’ll argue that it does not. At best, the neuromatrix theory yields identification of a mechanism implicated in the experience of any salient, bodily event. The theory does not identify a whole, with organised components, whose activities explain or determine pain. Consider Melzack’s neuromatrix as developed in his 2001. He writes (p. 1379), the body-self neuromatrix is a “… large, widespread network of neurons that consists of loops between the thalamus and cortex as well as between the cortex and the limbic system”. Though these loops carry separate streams of neural information, they also regularly converge and synthesise. The synthesis of repeated patterns of processing is called a neurosignature. This signature, he then claims (p. 1379), “… is imparted on all nerve impulse patterns that flow through [the neuromatrix]”. Different neurosignatures are supposed to represent different overall, unified bodily states. Melzack posits the different patterns activated across the body-self neuromatrix encoded in the signature as explaining the different qualities experienced as happening to the body at different times. The unified experience of an embodied self is then explained by a projection of neural information stamped with the neurosignature to yet other areas of the brain. In the model, the areas receiving this projection are labelled as the “sentient neural hub”. Here the stamped information—somewhat mysteriously, to my mind—is “converted” into awareness. Projection of the neurosignature from the matrix to yet other neural networks is posited as explaining both movement (e.g. spinal reflexes) and the experience of movement. Note two particular features of the model. First, the initial spatial distribution of the matrix’s loops is genetically determined, and both

116  Mechanistic Explanations the distribution and the patterns of information processing carried out across the loops become yet further individualised in response to sensory inputs throughout each individual’s life. Accordingly, each neurosignature is highly idiosyncratic, even in the face of identical stimulation. Your neurosignature, as we might put it, reflects both your genetics and your previous experiences; these alter the way that your particular brain processes the incoming information about what’s happening to your particular body. This processing then determines what it is like for you to experience your body on a particular occasion. The theory’s central thesis is that projected neural information “stamped” with your neurosignature will be experienced as yours, constituting your subjective experience of a unified, embodied self. Second, notice that pain is explicitly intended to be one subjective bodily experience among many—tickles, orgasms, itches, touch, and more are all, likewise, subjective experiences of a unified, embodied self. Each such experience is stamped with a distinctive neurosignature, which is posited to explain the qualities of your distinctive, subjective experience of your body. Applied to the experience of pain in particular, Melzack (2001, p. 1381) summarises the theory this way: The neuromatrix theory of pain proposes that the neurosignature for pain experience is determined by the synaptic architecture of the neuromatrix, which is produced by genetic and sensory influences. The neurosignature pattern is also modulated by sensory inputs and cognitive events, such as psychological stress. It may also occur because stressors … act on stress-regulation systems … thereby contributing to the neurosignature patterns … The neuromatrix theory guides us … toward the concept of pain as a multidimensional experience produced by multiple influences. These influences range from the existing synaptic architecture of the neuromatrix—which is determined by the genetic and sensory factors—to influences from within the body and from other areas in the brain. The following mechanistic sketch is offered17 (Figure 3.6): Note Two Further Features of the Theory as Summarised and Schematised. First, a wide range of things are offered as relevant to the resultant experience—including as relevant to whether the resultant experience is a pain. Melzack sometimes writes as if not only all sensory information, but all cognitive processing is causally relevant to the resultant neurosignature, i.e. to the qualities of your distinctive, subjective experience of your body, at any given moment of processing. This increases the idiosyncrasy of whether a particular person undergoes pain (or some other bodily experience) on a particular occasion, and relatedly increases the difficulty in offering a mechanistic explanation for why pain—and not some other experience—is had on any given

Mechanistic Explanations  117

Figure 3.6 Melzack’s Pain Neuromatrix.

occasion. The idiosyncrasy of token pains is further considered below and in the following chapters. Second, notice that the neuromatrix theory of the body-self retains the same three components included in the gate-control theory of pain: sensory- discriminative, affective-motivational, and cognitiveevaluative. These components—labelled in the schematic: ‘S’ for sensory, ‘A’ for affective, and ‘C’ for cognitive—are now taken to be captured by the activity of the neuromatrix. According to Melzack, every unified experience of the body-self has all three components. The interactions between the components are crucial determinants of the structure of each experience. Again: whether an experience is a pain experience depends on the particular, individualised neurosignature encoded by the neuromatrix on the neural information flowing through the matrix at any given time. The body-self neuromatrix does not yield a mechanistic explanation for pain. First, like others we’ve seen above, the schematic is at least currently far too schematic: we do not yet have a clear identification of parts, which ae organised and do things, such that their activities explain pain. It’s not clear that Melzack himself is appropriately interpreted as even aiming to eventually offer any such thing; his earlier claims that pains are so diverse as to defy definition are consistent with each pain resulting from some activity or other in the broadly sketched neuromatrix. More centrally, Melzack has, at best, identified a mechanism whose activity determines subjective, qualitative experiences of the body, but there is no identification here of the determinants of pain. As with Craig and his homeostatic system, Melzack does not even attempt to identify any components, organisation, or activities particular to pain as against any other bodily experience. So too, notice that while the

118  Mechanistic Explanations body-self neuromatrix was explicitly posited to facilitate explanations of bodily experiences which could not be explained by the gate-control theory, Melzack is not rejecting gate-control theory. He is supplementing it. What I think this reveals is that we may again do best to refrain from thinking of Melzack as even intending to identify the pain mechanism, and as instead identifying yet another mechanism whose activities may be usefully indicated as a potential treatment target in response to some pain reports. As noted above, the neuromatrix has received increasing attention in pain science and we should consider its contemporary discussion by other theorists. While Melzack uses the expression ‘the neuromatrix theory of pain’ in the quoted passage, he nowhere refers to it as the pain neuromatrix. Others soon began to do so, however, with ‘body-self neuromatrix’ all but falling out of use. Pain researchers soon began to disagree about the relationship between the neuromatrix and pain—Melzack’s own view being one among many. On one end of the spectrum were those who considered the matrix to have specialised components for pain (e.g., Rainville, 2002). Others at the somewhat opposite end held that particular activations across the matrix merely contributed to pain experiences (e.g. Tracey & Mantyh, 2007). Though the theory remains centre stage, evidence against its being appropriately considered the pain neuromatrix has been steadily accumulating. Mouraux et al. (2011) establish, conclusively to my mind, that when saliency is controlled, activity in the neuromatrix is at best somatosensory-specific, i.e. it is at best specific to bodily related feelings, but not to pain. As against the idea that activity in the neuromatrix is specific for pain, they conclude (p. 2247) that “… the ‘pain matrix’, can also respond to any salient or behaviorally relevant stimulus…”. Similarly, Legrain et al. (2011) conclude that responses in the neuromatrix reflect the body’s response to all salient sensory events—including those perceived as threatening prior to any experience the subject would report as pain (e.g. an approaching bee). In summary, the evidence seems to suggest that the activity in the neuromatrix at best determines salient experiences, perhaps bodily ones in particular, but its activities are not particular for pain. Even if the body-self neuromatrix is not the pain mechanism, or system, might some particular subset of components, organisation, or— most likely—activities within the matrix yield a mechanistic explanation for pain? Optimism that the theory would eventually deliver such an explanation was apparently rather widespread around the turn of the twenty-first century. Roy and Wager (2017, p. 89) summarise the original optimism attached to the theory this way: “…it was thought that each part of the pain matrix mapped onto different aspects or qualities of pain (e.g. localization, intensity, unpleasantness, motivation, etc.), and that their combined activation is what creates the full experience

Mechanistic Explanations  119 of pain”. But this optimism has increasingly appeared to be misplaced. Legrain et al. (2011), for instance, list and briefly describe a number of recent studies that support rejecting the claim that pain experience is represented by a specific pattern of activation within the matrix. Similarly, in considering a wide range of evidence, Roy and Wager note (2017, p. 89): … there is no evidence that any of the regions, or combinations of regions, of the pain matrix is specific to pain. Indeed, several brain-imaging studies have shown that most, if not all, structures of the pain matrix are sensitive to different kinds of salient events that are not necessarily painful… They take the evidence to suggest that the neuromatrix is best understood as a system dedicated to processing any salient events, with no activities within that system specific to pain. Their considerations lead them to write (p. 90):“…how can the experience of pain, which we feel as distinct from other salient events (e.g. receiving an unexpected reward), be caused by non-specific activity in a general salience-processing system? Our view is that it cannot”. Not only, then, is there currently no evidence to suggest that pain can be explained by some particular components or activities within the neuromatrix, there is evidence which suggests that pain is decidedly not thereby explained. Accordingly, even if granted, the neuromatrix theory does not yield a mechanistic explanation for pain. Though one may think there is some range of activities in the matrix that we will eventually identify which can explain pain, we currently lack any such identification. Moreover, evidence from considering the activities of the neuromatrix suggests that optimism for eventually identifying any such pain-specific activities within the network is misplaced. The moral of the section is that, even if granted, the neuromatrix theory of pain, like those theories of pain which have come before it (at least currently), fails to identify a pain system, or mechanism, whose workings explain pain.

3.6 Why There Are, At Best, Distinct Mechanistic Explanations for Distinct Pain Types The previous four sections surveyed four models of pain which have dominated pain science for the last 50 years. I argued that none of these, even if accepted, identify a mechanism whose workings explain pain. We do not currently have a mechanistic explanation for pain. There is—to date—no identification of a pain mechanism or system. The fact that we currently lack a mechanistic explanation for pain, however, doesn’t rule out two other relevant possibilities. First, the possibility that we will eventually have one. Though extant dominant

120  Mechanistic Explanations accounts fail to identify a pain mechanism, we may remain optimistic that some future identification will succeed. Many pain researchers in both science and philosophy seem to think that there simply must be some pain system, even if we can’t yet identify it. Second, even if identification of a mechanism for pain, as such, is not in the offing, we might think that mechanistic explanations for particular types of pain are nonetheless feasible. We may even think that some of the models discussed in previous sections will, eventually, provide these. Maybe some particular range of activities in certain areas of the neuromatrix, for instance, determine some particular types of pain, e.g. headaches. Perhaps, as another instance, some range of activities, or distinct set of components, in Craig’s posited homeostatic system can explain some other particular types of pain, e.g. burning pain. To address these two possibilities for mechanistic explanations of pain or pain types we turn to the research on the latter. In this section, I argue that the research on pain types rules out the first possibility: research into the different purported pain types reveals that they are explained by the activity of distinct and independent mechanisms. At best, then, there are mechanisms whose workings determine, or explain, distinct types of pain. In the concluding section, however, I’ll argue that our best evidence likewise supports rejecting even this possibility: research into the different purported pain types reveals that these, too, are explained by the convergence of activity in multiple, independent mechanisms. Moreover, and crucially, this convergent activity is idiosyncratic. The mechanistic determinants of each pain are particular to individuals on distinct occasions. I argue that the convergent, idiosyncratic activity which explains each token pain undermines mechanistic explanations of purported pain types. Before Turning to Research Concerning Pain Types, Two Preliminaries Are in Order. First, while I’ve distinguished between tokens and types throughout the previous chapters, as that distinction is about to come centre stage, it’s worth making my intended usage more explicit. As ever, I aim to be as liberal as possible. Tokens are particular, individual things. Types, by contrast, are—as I’ll think of them—kinds, or classes, of particular things. The same particular, individual thing can be a token of many types. I, for example, am one token of the types: human, wife, and sister. Types have many tokens: there are many tokens of each of the types mentioned in the previous sentence, i.e. many humans, wives, and sisters. Relatedly, the same collection of tokens may constitute different collections of tokens of different types—that is, we can individuate things differently. One and the same collection of things, for instance, may contain 10 tokens of the type pen, 5 tokens of the type red pen, 2 tokens of the type blue pen, and 3 tokens of the type orange pen. Exactly what types are, and in particular whether they are additional

Mechanistic Explanations  121 things which exist over and above their tokens, is a matter of heated philosophical controversy that has received significant attention.18 Philosophers sometimes ask: does the type of thing, Wife, exist over and above all the particular, token wives? Or again: is there a type of thing, pen, which exists over and above all the particular token pens? I myself am sceptical. But my scepticism won’t matter for anything I’m up to in this book. My talk about types here is entirely non-committal; everything I say should be consistent with thinking about types, and tokens, in any way you like consistent with the liberal definition with which this paragraph began. We’ll be asking whether some pain types—some groupings, collections, or classes, of particular tokens of pain—are subject to a mechanistic explanation which explains them (this chapter) and whether they—as a group, collection, or class—are usefully referenced in scientific generalisations for explanation and prediction (the next chapter). My arguments for negative answers to these questions do not rely on any controversial claims about the metaphysics of types—e.g. whether there is some type, headache, which exists over and above all the headaches.19 Second, many different distinctions are currently used to classify types of pain for research and diagnostics. In this section, I’ll use what I take to be a standard classification of pain types: nociceptive, inflammatory, and chronic pain. Distinguishing in this trifold way: nociceptive pain is, roughly, acute pain, i.e. pain of brief duration, caused by damage or injury; inflammatory pain is, roughly, acute pain caused by inflammation and the related release of certain chemicals; chronic pain is, roughly, pain of long duration. What is known about these three pain types shows that identification of a mechanism which explains all pain is not in the offing, i.e. there is no pain system. Additional classifications are usually yet more fine-grained, i.e. more specific, adding further types of pain that fall within one of the three broad types in the standard classification here used. If the three types considered here are not subject to a mechanistic explanation, the same will go for the more fine-grained types that they include. Alternatively, if less commonly, some pain types are taken to implicate mechanisms such that they cross-cut the broad types I focus upon; that is, there may be some ways of grouping pain into types such that some token pains may not appropriately fall into any of these three types. Luger et al. (2005), for instance, argue that bone cancer pain implicates the activity of unique mechanisms with components similar to both inflammatory and neuropathic pain, but different enough that bone cancer pain is inappropriately classified as either. Any additional pain types like these are of no concern for my purposes; again, the three types of pain we consider here are enough to show that there is no mechanism for pain as such. Similar considerations apply to distinct classificatory systems. Sometimes, for instance, pains may be

122  Mechanistic Explanations alternatively classified as acute and chronic nociceptive pain, which are contrasted with acute and chronic neuropathic pain. Considering and contrasting yet further types will only strengthen the argument of the current section: that distinct, independent mechanisms are needed, at least, to explain distinct pain types. Whether pain types themselves are subject to mechanistic explanation is considered in the following section. Scholz and Woolf’s (2002) is an exemplary article for present purposes. They distinguish between nociceptive, inflammatory, and neuropathic pain in taking up their article’s eponymous question ‘Can we conquer pain’. The authors note (p. 1062) that while we use a single word ‘pain’ to refer to a wide range of experiences, ‘this does not mean that pain is a monolithic entity’. They advocate splitting pains into three distinct types (p. 1062) for explicitly mechanistic reasons: Nociceptive, inflammatory and neuropathic pains result from diverse mechanisms. Some of these mechanisms are unique to one pain condition; others are present in multiple clinical syndromes, or may be expressed at different times during the natural history of a syndrome. Standard mechanical models of each pain types are provided by the authors and represented in Figure 3.7.20 The details of these models are not relevant, but the clear differences between the sketched mechanisms are crucial. Though all include nociceptors, the dorsal horn, and the brain, each also represents different activities in these regions and additional (distinct) entities and activities. If the models presented here are accurate, they are enough to show that different pain types implicate different mechanisms. There are distinct wholes with distinct parts that are distinctly organised and doing distinctive things such that their organised activities—even potentially— distinctly explain these distinct pain types. In short: the mechanism(s) implicated in chronic pain are distinct from the mechanism(s) implicated in nociceptive pain or inflammatory pain. Again, the very reason the authors distinguish these three types of pain is the distinctness of the mechanisms which they take to explain the tokens of those types. There is no monolithic pain mechanism or pain system: there are, at best, distinct systems and mechanisms for distinct pain types. 21 For doubters maintaining that there must be a pain mechanism and that we should keep trying to find it, the most effective line of refutation may be to emphasise treatment. Consider the distinct pharmacological treatment options presented in the models above. Notice that none are even provided for nociceptive pain—reflecting that pharmacological treatment of nociceptive pain is, at least usually, inappropriate. That tokens of different pain types require different treatment interventions is common sense. Consider the absurdity, for instance, of taking an aspirin

a

Nociceptive pain

Pain Avoidance Emotional reaction

TRPV1 TRPV2 TRPV3 TREK-1

DRG (cell body)

TRPV1 ASIC DRASIC

Acid

Withdrawal MDEG DRASIC TREK-1

Spinal cord

TRPM8

b

Inflammatory pain

Mast cell

Macrophage

Histamine Serotonin Bradykinin Prostaglandins ATP

c

Neutrophil granulocyte

H+ Nerve growth factor TNFα Endothelins Interleukins

Pain treatment options: Cox2 inhibitors Opioids

Neuropathic pain Spinal cord injury

Carpal tunnel syndrome

Thalamic stroke

Pain treatment options: Tricyclic antidepressants Anticonvulsants Na+ channel blockers NMDA receptor antagonists Opioids Debbie Maizels

Figure 3.7 Mechanical models of nociceptive, inflammatory, and chronic pain.

124  Mechanistic Explanations for the pain caused by a paper cut. With perhaps no understanding of what any of the implicated mechanisms may be, you take certain drugs for stomach pain and others for headaches. Different treatment interventions for different pain types are more likely to be effective, because distinct treatment interventions target distinct mechanisms. (We’ll see in the next section and the following chapter why targeting a mechanism typically implicated in a pain type is woefully sometimes nonetheless not an effective treatment.) Recall that, for pain science, treatment is the crucible for theory: a mechanistic explanation of pain should facilitate explanations and predictions that are useful for effectively treating pain. Scholz and Woolf (2002) are clear that the reason for privileging the involvement of different mechanisms in distinguishing different pain types is to facilitate more adequate treatment interventions: tokens of these three pain types are not determined by the workings of a single mechanism and, therefore, have different treatment targets. Adequate treatment is only possible if we recognise the role of these distinct mechanisms in these distinct pain types. Again, this is something that we typically recognise in our everyday lives: in at least most cases, you shouldn’t take an antacid for a headache or a burn on your hand. Scholz and Woolf, moreover, are explicit that the different mechanisms identified undermine the search for a single pain mechanism which may serve as an appropriate treatment target. They write (2002, p. 1065, emphasis added): The notion that there is a class of drug, a universal analgesic, that can intrinsically reduce all pain, is obsolete and has to be abandoned. Pain is heterogeneous in terms of etiological factors, mechanisms and temporal characteristics. Consequently, treatment must be targeted not at the general symptom, the pain, or its temporal properties, acute or chronic, but rather at the underlying neurobiological mechanisms responsible. Distinct mechanisms are implicated in, at least, distinct pain types. Accordingly, these distinct pain types, at least, require distinct treatment interventions. While the existence of a universal analgesic may provide some support for a pain mechanism, there is no evidence that there is any such analgesic or any such mechanism.22 Recall also Wall’s claim that the question ‘pain or no’ is diagnostically inert. No diagnosis can be provided on this basis. No treatment intervention is illuminated—indeed, as for nociceptive pain as represented above, sometimes the appropriate response is no intervention. The diagnostic utility of the pain report depends entirely on the provision of further information: where it hurts, how long it has hurt, what caused the pain, the further sensory and affective qualities of the episode, the threat of the injury, whether there is an injury, and yet more. Reporting

Mechanistic Explanations  125 pain, without further details about the token pain—its location, intensity, etiology, and other qualities—is diagnostically useless. It doesn’t even indicate whether any intervention is appropriate. One reason for the diagnostic impotence of the simple pain report, as we can now see, is that different mechanisms are appropriately targeted in distinct cases. The more we investigate, the more we find different mechanisms are implicated in (at least) different types of pain, undermining the prospects of eventually identifying a pain mechanism or system. It is what we already know about the mechanisms implicated in purported pain types which allows us to conclude against any eventual mechanistic explanation of pain as such. Our brief consideration of even the three broad types of pain from the standard classification is sufficient to make this point. The distinct and independent mechanisms schematised above are amply evidenced and widely—nigh universally—accepted. The multiplicity of implicated mechanisms for distinct pains is perhaps most clearly evidenced by focussing on treatment: the goal of pain science and any mechanistic explanation of pain. The general type, pain, is diagnostically inert, and there is no universal analgesic which targets a pain mechanism whose workings determine all pain. Instead, corresponding treatment interventions for, at least, distinct pain types target distinct mechanisms implicated in distinct pain types. That different treatment interventions are at least usually appropriate for distinct pain types is evidenced even by common sense. What we already know about the different mechanisms and treatment targets implicated in different pain types undermines the prospects of any future identification of a pain mechanism or system which explains all pain. I conclude that there is no pain mechanism or system. There are, at best, distinct mechanisms for distinct pain types.

3.7 Why There Are No Mechanistic Explanations for Distinct Pain Types We turn now to whether any pain types are subject to mechanistic explanations. I argue that they are not. In the previous section, I allowed that token pains could be grouped into types in any way that one wished. We considered a standard tripartite classification, but any would work for arguing against a mechanistic explanation for pain as such. To see why there are no mechanistic explanations for pain types, however, it will be helpful to first consider how pain classification has in fact proceeded. How have we tried grouping token pains into pain types? As briefly discussed in Chapter 1, until recently, pain classification was driven by the disease, or medical, model of pain which prevailed in pain research and diagnostics. The model emphasised the presumed explanatory role of diseases or pathologies—roughly, problematic structural

126  Mechanistic Explanations or functional bodily abnormalities. 23 Each distinct, token pain was presumed to have a pathological origin whose removal would eliminate the pain. The centrally relevant assumption for present purposes is that distinct pathologies explain, or determine, distinct pain types. Token pains were accordingly to be grouped, i.e. typed, by pathology. Though the medical model was motivated by the goal of facilitating effective treatment, it has been widely rejected for its failure to do so. A patient presenting with pain was to be diagnosed such that the presumed pathological origin of their pain was identified and, whenever possible, eliminated. Eliminating the pathology was supposed to eliminate the pain. The problem, in short, is that pathologies and pains only poorly correspond. 24 The qualities, intensity, location, and very presence or absence of pain varies across patients with the same pathology. Patients with similarly reported pains have a variety of pathologies—including, sometimes, no pathology. These variations are of course a serious problem for using a classification of pain types based on pathologies for any treatment purposes. Some token pains are determined by an underlying disease or pathology, such that eliminating the pathology eliminates the pain. Many, however, simply are not. Eliminating the pain is thus a distinct goal from eliminating the pathology. Using distinct pathologies to classify token pains into distinct types fails because pains and pathologies poorly correspond. More generally, though etiology, pathology, history, and responsiveness to treatment have all been tried and are sometimes deployed in pain science and medicine for classifying token pains into types, all are now widely recognised to be similarly problematic. Indeed, the inadequacies of these traditional approaches are recognised even by those who continue to use them. 25 Enter mechanisms. In hopes of greater success, many in the last 20 years have begun turning towards the mechanism-based classification of pain introduced in Chapter 1. Recall that this alternative approach, sometimes dubbed ‘pain analysis’, seeks to group pains into types based on mechanism types. Even as the core assumption of the medical model is that distinct pathologies explain, or determine, distinct pain types, the core assumption of mechanism-based classification is that distinct mechanisms explain, or determine, distinct pain types. We no longer seek to eliminate the pain by eliminating some presumed explanatory pathology; rather, we seek to eliminate the pain by manipulating the workings of some presumed explanatory mechanism. In their landmark paper, Woolf et al. (1998) identify four criteria for evaluating the adequacy of a mechanism-based classification of pain: reliability, validity, generalisability, and comprehensiveness. These criteria are referenced by most adopters of the mechanism-based approach. Reliability requires (1998, p. 228) that the classification provides “truly operational criteria” and includes appropriate “inclusion and exclusion

Mechanistic Explanations  127 criteria”. The basic idea is that the classifications need to illuminate mechanistic targets whose manipulations do not manipulate either too much or too little. Currently, for instance, the so-called ‘pain-killers’ typically affect much more than pain. Consider opioids. There are opioid receptors throughout the nervous system, and opioids have a widespread effect on functioning. Consequently, opioids not only often eliminate pain, they eliminate whole swaths of functioning and induce additional sensory and affective mental episodes. Thus, as most of us are all too vividly aware, opioids like oxycodone (common brand: OxyContin), hydrocodone (common brand: Vicodin), codeine, and more besides are often imbibed for effects besides pain elimination. Other interventions such as antidepressants for chronic pain, as another example, can affect both too much and too little: all too often, in such cases, many other aspects of the patient’s functioning are altered without eliminating the pain. Validity is defined (1998, p. 228) as “…an estimate of the degree to which the classification system corresponds to the underlying biology of the disorder being studied”. Since there is no “gold standard” for this in pain research we are encouraged (1998, p. 228) to “…use an iterative, fallible process of searching for and identifying symptom clusters, biological markers, history, and treatment response”. If this sounds vague, that is because it is. The basic idea is that though we have rejected the medical model on the grounds that correlation between pain as reported and any identifiable biological marker is poor, we should nonetheless aim for an estimate of the role that any biological marker may play in explaining the tokens of any pain types included in the classification. Perhaps, the idea goes, some pain types are more closely tied to pathologies or particular biological markers than others. The final two criteria are more straightforward. Generalisability requires that the classification apply to every token of the pain type. Comprehensiveness requires that there are no token pains left out of the classificatory schema—a major problem, as we’ve seen, with monolithic theories of pain. No one has yet provided a mechanism-based classification of pain that comes anywhere close to satisfying these criteria. Going further, at the moment, we cannot even begin to apply such criteria because we lack the requisite identified correlations between clusters of symptoms and corresponding mechanisms. Correlating symptoms with mechanisms is the centre of the mechanism-based approach as presented, for instance, by Woolf and Mannion (1999). We are to measure symptoms, as they are presented in the clinic, to identify mechanisms to target for treatment. We are nowhere near successfully doing any such thing for pain. Recall from Chapter 1 that Woolf et al. (1998) initially proposed three pain types—transient pain, tissue injury pain, and nervous system injury pain—and possibly correspondent, explanatory, mechanisms. It was hoped that these correspondences would eventually be tightened and

128  Mechanistic Explanations that classificatory schemas could then be tested against the criteria offered above to yield yet further tightening. So far, however, the approach has continued to fall at the first hurdle. As problematic as the medical, or disease model is now recognised to be, and however theoretically compelling we may find the new mechanismbased approach, we cannot yet successfully implement it in practice. We continue to lack identified correlations between groupings of token pains based on symptoms and any distinct identifiable mechanisms. Advocates of the approach have been consistently explicit about the need to correlate symptoms with mechanisms to use the approach, but also about our inability to do so. Recall once more, from Chapter 1, the lament of Finnerup and Jensen (2006, p. 113), having laboured to identify a mechanism which explains or determines even a single candidate pain type (their particular focus is neuropathic pain): • •

• •

To develop an effective mechanism-based classification, we need to be able to relate symptoms and signs to mechanisms and to identify specific treatments for specific mechanisms. One mechanism might give rise to different symptoms or signs; for example, upregulation of sodium channels in C-fibres increases fibre activity, resulting in burning pain, paroxysms, and dynamic mechanical allodynia. Similarly, one symptom or sign can be caused by several initiating mechanisms; for example, cold allodynia can be attributed to different mechanisms in peripheral and central neuropathic pain. It is becoming clear that we have not yet obtained a viable mechanismbased classification for neuropathic pain, and more rigorous studies are required to test this approach.

Again: the double dissociations between symptoms and signs, and underlying mechanisms, even within types that we have attempted to construct, remain a major problem facing the mechanism-based approach. In considering a range of examples evidencing dissociations between the workings of a mechanism and pains as reported, long-time advocates of the mechanism-based approach Jensen and Baron (2003, pp. 2–3) similarly lament: “Most likely symptoms, signs and mechanisms are related, but probably not directly. …symptoms and mechanisms involved in a particular pain condition cannot always be predicted. Is it then impossible to dissect pathophysiological mechanisms? It is probably not possible”. Both advocates and antagonists of the approach recognise that we currently lack identifications of the needed mechanistic correlations. Though we currently lack mechanistic explanation of pain types, might we nonetheless succeed? In the remainder of this section, I argue that the answer is no. Offering mechanistic explanations for pain types requires groupings of token pains which correspond to some mechanism

Mechanistic Explanations  129 which determines them. We now know, however, that each token pain is instead determined by the convergent activity of multiple mechanism, and, crucially, this convergence is idiosyncratic. The idiosyncratic complexity of pain undermines attempts to classify groups which correspond to the workings of an explanatory mechanism. Note that the claim that pain types are not mechanistically explicable is not here offered as a prediction about what pain science may or may not achieve; rather, it is supported by widely accepted results from within pain science. It is what we already know about the mechanisms implicated in token pains which allows us to conclude against any eventual mechanistic explanations of pain types. Even as it was scientific inquiries into pain types which revealed that optimism for identifying a pain mechanism was misplaced, so it is research into token pains which reveals that optimism for identifying distinct mechanisms for distinct pain types is likewise misplaced. There are no mechanistic explanations for pain types because each token pain is explained by the idiosyncratic convergent activity of multiple mechanisms. Consider first the multiplicity of converging mechanisms, followed by the idiosyncrasy of their convergence. Each token pain is the result of the convergent activity of numerous mechanisms—genetic, chemical, biological, neural, and social. Whether a particular individual experiences pain on a particular occasion is determined, or explained, by the combined activity of these multiple mechanisms. Perhaps as a result of the revolution in pain science begun in the 1960s, this is now almost universally agreed upon by pain researchers. It is evidenced in all leading theories of pain (even Craig’s more specific and less convergent theory), such that I am hard-pressed to choose a singular quote or reference supporting it. Here is one especially clear and relevant example of the claim as made by Smart et al. (2008, p. 6, emphasis added): The generation, modulation and perception of pain involves simultaneous parallel processing in multiple and interrelated body systems, and as such, any distinct categorisation based on mechanisms is to some extent artificial since pain is the result of many mechanisms. The extent to which varying combinations of mechanisms contribute to any patient’s pain state can alter and change with time. There can also be great variation between individuals, injury and syndrome. The activity in numerous mechanisms determines each token pain. The interaction between these mechanisms, moreover, is dynamic and differs across pathologies and across individuals. Knowledge of the activity of any single, identified mechanism will not yield successful explanation or prediction of pain. This passage likewise begins to hint at idiosyncrasy: the

130  Mechanistic Explanations products of the convergent mechanistic activity will vary depending on the other mechanisms involved in each particular case, resulting in great variation not only for the same injuries and pathologies, but across individuals. Indeed, the dynamic nature of the processing is such that there is variation in the relevant mechanistic activity for the same individual across time. Turn now directly to idiosyncrasy: the convergent activities of the multiple mechanisms determining each token pain are idiosyncratic. The mechanistic determinants and explanations of each particular pain— undergone by a particular creature, on a particular occasion—are thus highly distinctive. One way to illuminate the distinctive nature of each token pain is to focus on determinants of pain that are recognised to be highly idiosyncratic if anything is. Accordingly, briefly consider the cognitive component of pain and the role of genetics. As clearly seen in the sections above, all contemporary scientific models of pain recognise its cognitive component. Pain science amply supports that cognitions are not mere reactions to pain, but components of it. And cognitions—what a particular individual thinks, believes, desires, and so on—are highly idiosyncratic if anything else. Accordingly, the cognitive component of pain experiences fosters a strong case for the distinctive nature of each token pain. Someone with one set of cognitions may thereby undergo intense pain when subject to the same sensory stimulation, for example, that someone else, with another set of cognitions, was subject to without undergoing any pain whatsoever. The so-called placebo effects and nocebo effects amply attest to cognition’s central role in pain26: beliefs and expectations are a crucial component of pain and play a large role in determining its sensory and affective qualities. Adequately explaining pain requires recognising the determining, explanatory role of cognition. And cognition, I am here stressing, is highly particular to the individual cogniser. It’s idiosyncratic if anything is. Another route to appreciating the idiosyncrasy of token pains is to recognise the importance of genetic mechanisms. The search for ‘pain genes’ provides a nice case study of the idiosyncratic convergence of multiple mechanisms in explaining each token pain. This genetic research suggests that sensitivities to particular types of noxious stimulations are reliably correlated with genetic differences—at least in the mouse (Mogil et al., 1999a, 1999b, 2000; Lariviere, 2002). These genetic differences correlate not just with nociceptive pain, but five (and growing) proferred pain types. Insofar as individual genetic differences play a role in determining pain—and the evidence suggests they do—the determinants of pain are again evidenced to be individualised. Notice that these identified genetic differences will not alone yield a mechanistic explanation for pain or any pain type; explaining token pains requires taking account of the other mechanisms implicated in

Mechanistic Explanations  131 the pain and their interactions with the newly identified genetic mechanisms. The authors are rightly explicit that identifying pain genes is the job of identifying which genes are relevant to pain. The role of genetic mechanisms in explaining pain is thus always discussed in the modest terms of modulation. Here is one choice quote (Mogil et al., 2000, p. 803): A number of benefits are likely to derive from the study of pain genetics. First, the discovery of novel genes and the confirmation of known genes as being pain-relevant should spur targeted drugdiscovery efforts. Second, the elucidation of genetic polymorphisms rendering individuals with varied sensitivity to pain and its inhibition should allow idiosyncratic use of existing therapies, maximizing their effectiveness and minimizing side-effect liability. … It should be emphasized, however, that environmental factors, acting both alone and in concert with genotype, exert more overall influence on complex biological phenomena, such as pain, than do genes… thus, in addition to putting up with the pain required to decipher pain genes, the search for sociocultural and other non-genetic factors that influence pain susceptibility and response must be pursued with equal vigor. Identifying genetic mechanisms implicated in pain may illuminate important avenues for novel treatments, but these mechanisms will not alone yield mechanistic explanations for pain or any pain type. Indeed, the authors claim in the above passage that sociocultural and environmental factors—also highly idiosyncratic—are even more relevant than genetic factors. Numerous other relevant mechanisms have, of course, been identified throughout this chapter, and there are more which space precludes discussing. Many mechanisms are ‘pain-relevant’, and genetic mechanisms are evidenced to be among them. Each token pain is explained by the convergent activity of these multiple mechanisms on each occasion—and the convergence of this activity, along with the components and activities of many of the mechanisms themselves, is highly idiosyncratic. Indeed, though the consequences for mechanistic explanations of pain and pain types have not been appreciated, the idiosyncratic nature of the determinants of each token pain is in fact widely recognised in pain science. We have seen this recognition already in three of the four dominant models of pain considered in the above sections. In arguing that pain defies adequate definition altogether, Melzack and Wall claimed that each pain experience is unique. Price, more specifically, claimed that it is the particular meaning that each individual attaches to their particular experience which determines its qualities; the meaning that a stimulation has for a particular individual on an occasion will

132  Mechanistic Explanations determine whether it is unpleasant and threatening for them on that occasion—and, according to Price, those are necessary conditions for the person to be in pain. The neuromatrix theory of pain perhaps most clearly recognises idiosyncrasy by positing individualised neurosignatures to explain the qualities of our distinctive, subjective experiences of our own bodies. It’s important to emphasise that it is not only ‘odd’ cases of pain whose determinants are highly distinctive. Idiosyncrasy is not only important for explaining, for instance, chronic pain and neuropathic pain which we might think are abnormal. Focus on paradigmatic acute pains, i.e. acute pains experienced as the result of some brief, noxious stimulation presented in an antecedently painless state. Even when one puts their hand on the stove, gets chilli powder in their eyes, or hits their thumb with a hammer, idiosyncrasy in attendant pain looms— including whether there is any! Sometimes putting one’s hand on the stove, getting chilli in the eyes, and getting hit with a hammer won’t cause pain, and the qualities and intensity of the pains which are caused may vary considerably across individuals and for the same individual across times. Acute, nociceptive pains like these are also subject to a host of cognitive and environmental factors whose relevance is widely evidenced. 27 Genetics, memories, previous experiences, the functioning of the individual’s implicated sensory and affective mechanisms, and more besides, are all determinants of each pain—whether there is any pain, the qualities of the pain, whether and how the sufferer is motivated, and so on. An objection may have long been brewing. The above discussion emphasises individual differences, but isn’t it ignoring significant similarities? Won’t most anyone undergo pain when shot? Won’t most anyone undergo horrific pain if they are cut from stem to stern? For that matter, don’t we have reliable analgesics—i.e. interventions used to alleviate pain—used in surgery to keep people from undergoing pain for medical procedures which would otherwise be horrific? These sorts of considerations may lead one to suspect that there are enough similarities for mechanistic explanations of at least pain types, even if not pain as such. Idiosyncratic complexity should indeed not be overblown. Many people have many things in common genetically, chemically, biologically, and socially. As a single example, consider that for most people, most of the time, aspirin will help a headache. Why? Because aspirin, as above, targets inflammatory mechanisms. And most people have enough in common biologically, genetically, chemically, and socially that their idiosyncratic combination of relevant mechanisms will include activation of inflammatory responses when they have a headache. This mechanism is targeted by aspirin and so, in some cases: voilà, no more pain. Aspirin helps headaches often enough, for enough people that companies

Mechanistic Explanations  133 which make pharmaceuticals branded headache relievers can succeed. Similar considerations apply to other pain types and targeted treatment interventions. Enough idiosyncratic convergence remains, however, to undermine mechanistic explanations of not only pain as such, but even these pain types. Does what we know about aspirin and the inflammatory mechanisms which it targets show that we have a mechanistic explanations of headaches? Not by a long shot. Headaches continue to be one of the most befuddling pain types. We know inflammatory mechanisms are often implicated and aspirin targets these mechanisms. But we also know that inflammatory mechanisms are not the whole story. Indeed, we know this in everyday life, too—even if we describe it differently in everyday language. We know, that is, that sometimes, when we have headaches, aspirin does not help. For some people, moreover, aspirin never helps, and, for a good proportion of people, a sugar pill they believe to be an aspirin will help just as well. Why? Because other mechanisms are also involved every time anyone has a headache. Sometimes these other mechanisms have a stronger weight in determining a particular headache than they do in determining others. Many of these mechanisms are highly idiosyncratic and their particular convergence, on any particular instance, always is. Sometimes the pain simply will not abate until you, for instance, reconcile with that disgruntled co-worker. Sometimes it will not abate until you stop believing that it never will. Again, we can explain these humdrum facts by recognising that there are numerous mechanisms which determine each token pain and their convergence is highly idiosyncratic. Similar considerations apply to tokens of all other supposed pain types. People have enough in common genetically, biologically, socially, and more such that being shot or being cut stem to stern will usually cause horrific pain. But there will, even here, be some individual variability in the experienced pain. And there may be some instances—as a result of environment, genetics, cognition, and so on—where even these sensory stimulations will not result in pain. Going further, many of the interventions to avoid or alleviate what is likely to be horrific pain wipe out wide swaths of functioning. Opioids, for example, widely alter functioning across the nervous system as above discussed. General anaesthesia, of course, results in the subject feeling nothing whatsoever. Using the criteria offered by Woolf et al. for a classificatory schema discussed above, we can recognise these treatment interventions as lacking reliability for either pain or any pain type: they lack appropriate inclusion and exclusion criteria. Death, as the most extreme example, will eliminate pain, but this does not show that there is a reliably targeted mechanism whose workings explain pain or any pain type; death eliminates everything.

134  Mechanistic Explanations These considerations lead us directly to the consideration which perhaps illuminates the highly idiosyncratic determinations of each token pain more starkly than any other: treatment. The variability across token pain experiences, even when stimulation, injury, pathology, and implicated mechanisms are all held constant, is a well-known, practical hurdle faced by every clinician. As the explanation of token pains includes the genetic, molecular, chemical, biological, and social factors relevant to a particular individual’s pain, at a particular time, the determination and explanation of their pain is highly individualised. Accordingly, so too should be the treatment intervention. Thus, as every clinician is well aware: adequate treatment for pain must be tailored to the individual. Indeed, every parent is well aware of the need for individually tailoring their interventions in response to pain reports from their individual children. As treatment is the goal of pain research, the fact that it is individuals who must be treated cannot be overemphasised. Adequate treatment of individuals requires recognising the idiosyncratic complexity of pain. In closing this chapter, I want to emphasise the way in which the claim that pain is determined by the idiosyncratic convergence is situated in the developing history of pain science. Pain science has progressed from monolithic, simplistic views of pain to convergent views which recognise its multiple components. The dominant theories at the turn of the century held that pain was a specific, sensory phenomena: we believed in a specialised pain system with pain receptors, pain pathways, and pain cortical centres. Gate-control theory disillusioned us of this simplicity, by discrediting either that pain was a purely sensory phenomena or that it was subserved by the activities of any pain-specific components. In the wake of the freedom to recognise pain’s multiple dimensions, numerous mechanisms were discovered to be implicated in a wide range of pains. In attempting to group these pains first by pathology and then by mechanism, we have learned that not only are different mechanisms implicated in different pains, but that multiple mechanisms are implicated in each one. Moreover, we have learned that these mechanisms and their activity are highly idiosyncratic—genetics, memories, past trauma, cognition, and more must all be recognised if pains are to be explained and adequately treated. The rise of the modern pain clinic, centring on individualised, multidimensional treatments from a range of practitioners with multiple specialties bears witness to these developments. This is the history of pain science. It is on the basis of these developments in pain science that I have argued in this chapter that neither pain nor any pain type is subject to mechanistic explanation. It is what we already know about the mechanisms implicated in pain types which allows us to conclude against any eventual mechanistic explanations of pain as such. It is what we already

Mechanistic Explanations  135 know about the mechanisms implicated in token pains which allows us to conclude against any eventual mechanistic explanations of pain types. There is no mechanism for pain or any pain type. Instead, each token pain is the result of the idiosyncratic convergence of the activity of multiple mechanisms. Note finally, however, that we cannot conclude from this that there are no mechanistic explanations, or determinants, of each token pain. 28 The arguments presented here are certainly intended to be consistent with a naturalistic, physical, explanation for each token pain experience; for all I have here argued, we needn’t posit anything supernatural or irreducible to the physical to explain each token pain. Similarly, for all I have here argued, each token pain is mechanistically explicable. We might, for one instance, consider individual persons as a whole, and take their individual pains on particular occasion to be explained by the activities of the many systems which comprise their overall self. We are, after all, working with a very liberal notion of mechanisms or systems. Answering the broad question of whether we should think of individuals as mechanisms or systems (the activities of which may explain each token pain) takes us beyond what’s needed for present purposes, where our focus is on scientific generalisations. The central question here is whether reference to pain (as such) or pain types is useful for scientific generalisations—and that question remains whether each token pain is mechanistically explicable or not. In everyday life, we blithely recognise the idiosyncratic nature of pain— and respond to our own and others’ pain accordingly. The clinician, too, can recognise the particular, idiosyncratic nature of each particular pain and can tailor their treatments to the individual—indeed, if treatment is to be adequate, they must do so. Science, however, trucks in generalisations. Even if there are mechanistic explanations for individual token pains, science is not in the business of offering individualised explanations of tokens. Instead, scientific generalisations inevitably gloss over individual differences. The crucial question then becomes: might the discovered individual differences be negligible, such that generalisations about pain and pain types are useful for scientific explanation and prediction? Might we have a successful science of pain despite its complex idiosyncrasy? Accordingly, we now turn in Chapter 4 to whether pain science can survive the conclusion that each token pain is explained by the idiosyncratic convergence of multiple mechanisms. I argue that it cannot. The idiosyncratic nature of each token pain undermines the utility of reference to pain or pain types for scientific explanations and predictions. As long as we retain reference to the wide range of implicated mechanisms which idiosyncratically converge to explain each token pain, no scientific utility will be lost, and some will even be gained.

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Notes







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the space nor the expertise to settle these debates here. For our purposes, it is enough to evaluate whether even if Craig’s model is correct, it yields a mechanistic explanation for pain. I note, however, that Tommerdahl et al. (1996, 1998) provides evidence that Craig’s own particular termination area of interest in the parietal cortex, area 3a, appears to respond preferentially to all thermal stimulation—not only noxious thermal stimulation. This research implies that the area is therefore also not best understood as nociceptive or pain-specific—a conclusion that Craig himself needn’t resist, given that his emphasis is on homeostasis and not pain alone. Similar comments apply to the authors’ discussion of what they label emotional pain (pp. 106–107). Recall also, as discussed in text above, that the signals terminating in the insular cortex are taken by Craig to subserve the sensory, as against the motivational dimension of pain, and that these representations in the insular cortex must receive meta-representation in the anterior insula to constitute the experience of pain (see e.g. 2003a, p. 24). Craig thus apparently holds that what it is like for one to be aware of one’s pain—from the inside—is to be aware of a sensation of some kind as against (on his view) the motivation to do something. This also is apparently in seeming contrast with imperativism for pain or, presumably, even for itch. Reprinted with permission from Melzack (2001), permission conveyed through the American Dental Education Association. For an introductory overview, see Wetzel (2018). Of course, to know that a token is a token of some type, we have to have some prior idea about what that type of thing is. You can’t go around counting wives unless you already have at least some idea about what a wife is. We need individuation conditions. For our purposes: to identify a token pain requires some idea of what type of thing a pain is. As noted many times now, I take pains to be a posit of our everyday theory: it was everyday people going about their everyday purposes who began to pick out particular, individual things as pains. Accordingly, I take every reader to already have at least some idea about what type of thing a pain is, i.e. to have a fairly firm grip on the individuation conditions. Even though, as we’ve also noted, our everyday theory has its limits. Whether our everyday theory of pain is a good theory, such that we should accept its posit of pain, will be considered in Chapter 5. This footnote and the paragraph to which it is attached will undoubtedly fail to satisfy philosophers exercised about types, but I trust it is enough for everyone else, and is anyway sufficient for assessing all the arguments in text. Republished with permission from Scholz and Woolf (2002), permission conveyed through Copyright Clearance Center Inc. An anonymous reviewer of this manuscript was concerned that the distinct mechanistic explanations discussed in text inappropriately emphasise peripheral differences, whereas the pain mechanism is presumably exclusively a brain mechanism. In response, note first and most centrally that I am following pain science. It is inappropriate to presume from the armchair whether peripheral happenings are appropriately included in mechanistic sketches of pain. It is worth considering that the presumed pain mechanism historically included almost no role for central activity—consider again Descartes’ model in Figure 3.1. Whether we presume that there must be some pain mechanism in the brain that does not extend to any peripheral mechanisms or that there must be some peripheral mechanism that merely terminates centrally, the presumptions are presumptuous. What’s needed is empirical investigation. Second, following the science leads to the inclusion of central mechanisms—as indeed discussed in this chapter, e.g. the previous

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22

23 24 25 26 27 28

section on the neromatrix or the depiction here of the release of distinct neural chemicals—and throughout the book. What I am arguing in this chapter is that empirical investigation reveals that there are multiple mechanisms whose convergence idiosyncratically results in distinct token pains. There is no identifiable pain mechanism whether we focus on the periphery (as historically done, as with Descartes), solely centrally (as suggested we should do by the anonymous reviewer), or on both as with the currently dominant models discussed throughout the text. Edwards et al. (1999) is sometimes offered in support of the contention that aspirin is a universal analgesic. Their study, however, focusses only on acute, postoperative pain. For an extended discussion of why Edwards et al. (1999) does not establish that even all acute postoperative pains are explained by the same mechanism (or all appropriate treated by aspirin), see Chapter 42 of Wall and Melzack’s 2006 Textbook of Pain (Lopez 2006). See e.g. Carel and Cooper (2014) for worries about the very categories of disease or pathology. See again Chapter 1 and especially the quoted passage from Smart et al. (2008). For further discussion, see, for example, Hansson (2003). For overviews of such effects, see for instance, Benedetti et al. (2007) and Benedetti (2014). For an argument that lumping all such effects together into a single grouping of ‘placebo effects’ is problematic, see Corns (2018). In addition to the aforementioned references from the placebo and nocebo literature, see also some beautiful experimental work as discussed in Pennebaker (2012). I am grateful to Fiona Macpherson for discussion of this point.

References Benedetti, F. (2014). Placebo effects. Oxford University Press. Benedetti, F., Lanotte, M., Lopiano, L., & Colloca, L. (2007). When words are painful: Unraveling the mechanisms of the nocebo effect. Neuroscience, 147(2), 260–271. Carel, H., & Cooper, R. (2014). Health, illness and disease: Philosophical essays. Routledge. Corns, J. (2018). The placebo effect. In Philosophy of pain, D. Bain, M. Brady, and J. Corns (eds.). Routledge, 105–129. Craig, A. D. (2003a). Pain mechanisms: Labeled lines versus convergence in central processing. Annual Review of Neuroscience, 26(1), 1–30. Craig, A. D. (2003b). A new view of pain as a homeostatic emotion. Trends in neurosciences, 26(6), 303–307. Dallenbach, K. M. (1939). Pain: History and present status. The American Journal of Psychology, 52(3), 331–347. Easter, J. S., Purves, D., Rakic, P., & Spitzer, N. C. (1985). The changing view of neural specificity. Science, 230(4725), 507–511. Edwards, J. E., Oldman, A. D., Smith, L. A., Carroll, D., Wiffen, P. J., McQuay, H. J., & Moore, R. A. (1999). Oral aspirin in postoperative pain: A quantitative systematic review. Pain, 81(3), 289–297. Finnerup, N. B., & Jensen, T. S. (2006). Mechanisms of disease: Mechanismbased classification of neuropathic pain—A critical analysis. Nature Reviews Neurology, 2(2), 107.

Mechanistic Explanations  139 Hansson, P. (2003). Difficulties in stratifying neuropathic pain by mechanisms. European Journal of Pain, 7(4), 353–357. Hardcastle, V. G. (1999). The myth of pain. MIT Press. Jensen, T. S., & Baron, R. (2003). Translation of symptoms and signs into mechanisms in neuropathic pain. Pain, 102(1), 1–8. Klein, C. (2015). What the body commands: The imperative theory of pain. MIT Press. Lariviere, W. R., Wilson, S. G., Laughlin, T. M., Kokayeff, A., West, E. E., Adhikari, S. M.,…Mogil, J. S. (2002). Heritability of nociception. III. Genetic relationships among commonly used assays of nociception and hypersensitivity. Pain, 97(1–2), 75–86. Legrain, V., Iannetti, G. D., Plaghki, L., & Mouraux, A. (2011). The pain matrix reloaded: A salience detection system for the body. Progress in Neurobiology, 93(1), 111–124. Lopez, B. C. (2006). Wall and Melzack’s textbook of pain (No. 63). Churchill Livingstone. Luger, N. M., Mach, D. B., Sevcik, M. A., & Mantyh, P. W. (2005). Bone cancer pain: From model to mechanism to therapy. Journal of Pain and Symptom Management, 29(5), 32–46. Melzack, R. (1989). Phantom limbs, the self and the brain (the DO Hebb Memorial Lecture). Canadian Psychology/Psychologie Canadienne, 30(1), 1. Melzack, R. (2001). Pain and the neuromatrix in the brain. Journal of Dental Education, 65(12), 1378–1382. Melzack, R., & Wall P. D. (1988). The challenge of pain. 2nd ed. Reprint, London: Penguin Books, 2008. Mogil, J. S., Wilson, S. G., Bon, K., Lee, S. E., Chung, K., Raber, P., & Elmer, G. I. (1999a). Heritability of nociception I: Responses of 11 inbred mouse strains on 12 measures of nociception. Pain, 80(1–2), 67–82. Mogil, J. S., Wilson, S. G., Bon, K., Lee, S. E., Chung, K., Raber, P. & Elmer, G. I. (1999b). Heritability of nociception II: Types’ of nociception revealed by genetic correlation analysis. Pain, 80(1–2), 83–93. Mogil, J. S., Yu, L., & Basbaum, A. I. (2000). Pain genes?: Natural variation and transgenic mutants. Annual Review of Neuroscience, 23(1), 777–811. Mouraux, A., Diukova, A., Lee, M. C., Wise, R. G., & Iannetti, G. D. (2011). A multisensory investigation of the functional significance of the “pain matrix”. Neuroimage, 54(3), 2237–2249. Nagasako, E. M., Oaklander, A. L., & Dworkin, R. H. (2003). Congenital insensitivity to pain: An update. Pain, 101(3), 213–219. Pennebaker, J. W. (2012). The psychology of physical symptoms. Springer Science & Business Media. Porreca, F. (2015, June). Nociceptors, the spinal dorsal horn, and descending modulation. In Pain 2012 Refresher Courses: 14th World Congress on Pain. Wolters Kluwer Health Adis (ESP). Price, D. D. (1999) Psychological mechanisms of pain and analgesia. IASP Press. Price, D. D. (2000). Psychological and neural mechanisms of the affective dimension of pain. Science, 288(5472), 1769–1772. Price, D. D. (2017) A view of pain based on sensations, meanings, and emotions. In Routledge Handbook of Philosophy of Pain, J. Corns (ed.). Routledge, 113–223.

140  Mechanistic Explanations Rainville, P. (2002). Brain mechanisms of pain affect and pain modulation. Current Opinion in Neurobiology, 12(2), 195–204. Roy, M., & Wager, T. D. (2017). Neuromatrix theory of pain. In Routledge Handbook of Philosophy of Pain, J. Corns (ed.). Routledge, 87–97. Scholz, J., & Woolf, C. J. (2002). Can we conquer pain? Nature neuroscience, 5, 1062. Smart, K. M., O’Connell, N. E., & Doody, C. (2008). Towards a mechanismsbased classification of pain in musculoskeletal physiotherapy? Physical Therapy Reviews, 13(1), 1–10. Strigo, I. A., & Craig, A. D. (2017). “A neurobiological view of pain as a homeostatic emotion.” Routledge Handbook of Philosophy of Pain, J. Corns (ed.). Routledge, 98–112. Tommerdahl, M., Delemos, K. A., Favorov, O. V., Metz, C. B., Vierck Jr, C. J., & Whitsel, B. L. (1998). Response of anterior parietal cortex to different modes of same-site skin stimulation. Journal of Neurophysiology, 80(6), 3272–3283. Tommerdahl, M., Delemos, K. A., Vierck Jr, C. J., Favorov, O. V., & Whitsel, B. L. (1996). Anterior parietal cortical response to tactile and skin-heating stimuli applied to the same skin site. Journal of Neurophysiology, 75(6), 2662–2670. Tracey, I., & Mantyh, P. W. (2007). The cerebral signature for pain perception and its modulation. Neuron, 55(3), 377–391. Wetzel, L. (2018) Types and tokens. The Stanford Encyclopedia of Philosophy (Fall 2018 Edition), Edward N. Zalta (ed.). Elsevier, . White, K., Targett, M., & Harris, J. (2018). Gainfully employing descending controls in acute and chronic pain management. The Veterinary Journal, 237, 16–25. Woolf, C. J., Bennett, G. J., Doherty, M., Dubner, R., Kidd, B., Koltzenburg, M. & Torebjork, E. (1998). Towards a mechanism-based classification of pain? Pain, 77(3), 227–229. Woolf, C. J., & Mannion, R. J. (1999). Neuropathic pain: Aetiology, symptoms, mechanisms, and management. The Lancet, 353(9168), 1959–1964.

4

Adopting Scientific Eliminativism How Complex Idiosyncrasy Undermines Scientific Utility

4.1 Introducing Scientific Eliminativism The previous chapters have argued that pain—as posited by our everyday theory—is a complex phenomenon, with multiple and dissociating components. Each token pain—as revealed by scientific inquiry—is determined by the idiosyncratic convergence of the activity of multiple mechanisms. Put a bit less technically: the mechanistic activities which determine any particular pain vary from person to person, and indeed for the same person across times. Call this the complex idiosyncrasy of pain. In the previous chapter, I argued that the complex idiosyncrasy of pain is such that while there may well be mechanistic explanations of each token pain, the differences between the particular tokens undermine mechanistic explanations of pain types or pain as such. In the remaining chapters, we’ll further consider the implications of the complex idiosyncrasy of pain for science, everyday life, and medicine. This chapter directly focusses on the implications of complex idiosyncrasy for pain science. Put most generally, our question will be whether the complex idiosyncrasy of pain inevitably undermines pain science; more specifically, whether the complex idiosyncrasy of pain undermines the utility of generalisations about pain for scientific explanation and prediction. The worry that raises this heterodox suggestion is that science issues generalisations, but generalisations apparently require ignoring the idiosyncrasy of the complex convergent activity which explains each token pain. We’ll here consider whether the way in which pains differ from person to person renders it inappropriate to generalise about pain or pain types for scientific inquiry. Should we, instead, rid our sciences of any reference to pain or pain types—perhaps replacing these references, from case to case, with references to something else? Put more technically, our core question for this chapter will be whether pain or pain types are natural kinds. Recall that we are liberally taking natural kinds to be any kinds which are usefully referenced for explanation and prediction in scientific generalisations, i.e. we are using what I’ve dubbed the scientific utility criterion. The current question, then, is whether it is useful for explanation and prediction to refer to pain or pain types in scientific generalisations.

142  Adopting Scientific Eliminativism Before arguing for a negative answer to this chapter’s question, it’s worth backing up and introducing a few more technical terms to bring the question a bit more clearly into focus. Not all kinds are natural; not every kind is usefully referenced for explanation and prediction in scientific generalisations. Remember that we are liberally allowing that particular, individual things may be grouped together into kinds in any way that one likes. When we are this liberal about kinds, it’s obvious that not every kind is one about which science will usefully offer explanatory and predictive generalisations. As a toy example, consider the following grouping, or kind: the biggest potato, the smallest potted plant, and the most powerful politician— each from every country. We could give this kind a name: Postuff, say. Postuff is not subject to mechanistic explanation; there is no whole the parts of whose workings explain, or determine, Postuff. Going further, Postuff, I take it, is not a kind—that is, not a grouping of individual things—about which any science would appropriately inquire and about which it may offer useful generalisations. While potatoes, potted plants, and even politicians may all be groupings which are appropriately subject to scientific inquiry, i.e. while we may at least potentially offer generalisations about these kinds which are useful for scientific explanation and prediction, I trust that this is not the case for Postuff. Anything I may want to explain or predict will, presumably, be better explained or predicted using generalisations that don’t refer to Postuff. We may, for instance, want to predict or explain plants, politicians, or potatoes, when doing horticulture, economics, or botany, but I presume that attempted generalisations which refer to Postuff, as such, will only get in the way of these scientific endeavours. I presume that for scientific explanations and predictions, we can come up with better, i.e. more useful, groupings than Postuff. We could, of course, try it out: we could test attempted generalisations about Postuff. But I don’t recommend it. There is no reason to think it’s a useful grouping for scientific inquiry—indeed, I chose it as an example of something that I thought we may safely presume was not useful. The moral of the silly example is that while we may liberally allow that we can group things together into kinds in any way we like, not every such kind will be a natural kind—even using the liberal scientific utility criterion. I now stipulate that if a kind is not usefully referenced in scientific generalisations for explanation and prediction, then that is a sufficient reason to eliminate reference to it from those generalisations. The idea here is the rather simple one that if it’s not useful for our scientific purposes to generalise about a grouping, then we shouldn’t do so when aiming to achieve those purposes. Continuing to use the scientific utility criterion, we may put this rather simple point more technically by saying that scientific generalisations shouldn’t refer to kinds which aren’t natural. Such references should, when discovered, be eliminated. Should we find

Adopting Scientific Eliminativism  143 any references to Postuff in any scientific generalisations, to keep with our silly toy example, those references should be eliminated. Note that the reasoning here is explicitly pragmatic: references to kinds which are not usefully referenced for scientific explanation and prediction should be eliminated precisely because they are not usefully referenced for this purpose.1 Call the position that references to a kind should be eliminated from scientific generalisations, and accordingly cease to be an object of scientific inquiry, scientific eliminativism. 2 We should, I take it, be scientific eliminativists about Postuff. Notice, however, that the reason for this needn’t be that Postuff doesn’t exist: after all, if potatoes, politicians, and potted plants exist, maybe we should go ahead and grant that Postuff exists, too. Notice that Postuff’s scientific utility problem also isn’t that there is nothing for which references to Postuff would be useful: it’s my hope that the references to Postuff in this introduction are useful! As against either of these two points, the reason we shouldn’t refer to Postuff when we’re offering scientific generalisations is that it’s not useful for the explanations and predictions that those generalisations are aimed at offering. It’s worth stressing that we can thus at least sometimes settle the question of whether we should eliminate reference to a kind from scientific inquiry without settling the question of whether the kind exists. As in the previous chapter, we are dodging the difficult question of whether or not kinds exist over and above their members. The question of whether Postuff exists is strange—frankly, it is a question that only philosophers ask. The biggest potato, the smallest potted plant, and the most powerful politicians—each from each country—exist. If so, it’s then a bit strange to go on to ask whether there is some further thing, POSTUFF, which exists over and above these. Not only is this a strange question, but it’s a difficult one. And notice that the difficulty doesn’t just come from the fact that our example is a silly toy one; whether some further thing, the kind CHAIR, exists over and above all the particular chairs is also a strange and difficult question. As noted before, I won’t here try to settle these strange and difficult philosophical questions. What I want to now stress instead is that they don’t need to be settled for present purposes. Whether or not POSTUFF exists, we have sufficient pragmatic reasons to conclude that we should be scientific eliminativists about it: references to Postuff aren’t useful for the explanations and predictions at which any scientific inquiry aims. For our purposes, we can focus right in on the utility of reference, without worrying about the metaphysics of kinds or types. The difficulties are of course not all avoided, however, since questions about whether we should be scientific eliminativists about a kind are difficult enough in their own right. Postuff is a silly toy example, for which the question of scientific eliminativism was intended to be easy.

144  Adopting Scientific Eliminativism When we look at the kinds which are actually referenced in scientific generalistaions, it is not easy to determine whether they are being usefully referenced for explanation or prediction. One obvious reason to be scientific eliminativist about a kind is if we discover that its members simply don’t exist. We used to think, for example, there was a kind of thing phlogiston—a chemical posited to explain why some things could not burn, whereas others could: things which had phlogiston in them could burn because of their phlogiston, and things which couldn’t burn, couldn’t burn precisely because they lacked phlogiston. We determined, however, that there is no such thing as phlogiston. Accordingly, we ceased to refer to phlogiston in our scientific generalisations. To be clear: progress wasn’t made by discovering that there was no kind of thing, PHLOGISTON, over and above all the particular instances of phlogiston. (Set aside what a strange thing the very idea of such a scientific discovery may be.) Instead, progress was here made by the discovery that there weren’t any instances of phlogiston in any of the things which burned. What we discovered was that no members of the posited kind existed. Once we determined that there were no members of the kind, references to it weren’t useful for explaining or predicting anything. We have so far been taking for granted that members of the kind pain exist, i.e. particular pains exist. While we consider the radical view that they don’t in the next chapter, in this chapter we’ll keep taking it for granted that they do—however, complex and idiosyncratic scientific inquiry has revealed them to be. Accordingly, we won’t be looking at the idea that pains don’t exist as a reason to adopt scientific eliminativism about them. While references to phlogiston were eliminated from scientific inquiry on the grounds that it was a posited kind determined to have no existing members, we’ll for now grant that pain and pain types are posited kinds which do have existing members. There are no instances of phlogiston, but we’ll continue to assume in this chapter that you really do sometimes undergo a pain, e.g. have a headache or stomachache. We won’t adopt scientific eliminativism for pain on these grounds. There are, however, at least two further reasons to adopt scientific eliminativism which concern the way that members of a kind (which exist) are grouped.3 We may, for instance, collect too many things together and offer generalisations about them as one unified kind, when—to get better scientific explanations and predictions of the members of they kind—they should instead be separated into many. Memory, for example, may turn out to be this way. It turns out that there are multiple different types of memory: semantic memory, episodic memory, declarative memory, and so on. It may well be that memory is best separated out into these different types for all scientific inquiries. It may, that is, turn out that references to memory, as such, should be eliminated from scientific generalisations, though references to the different discovered memory types

Adopting Scientific Eliminativism  145 should be retained.4 The problem here (if there is one) isn’t that there are no instances of memory; rather, it’s that the way we are grouping all of these instances together—into the type memory as such—isn’t useful. On the other hand, we may separate things out into too many groups when— to get better explanations and predictions concerning the members of the kind—they should instead be grouped together into fewer kinds. As an ugly example from history: we now recognise that persons of all races are members of the same species, i.e. homosapiens. Biology, for instance, can deliver some successful explanations and predictions that would be lost if we didn’t include members of all races as belonging to that same species. I take it to be an open question whether there are any references to races, as against references to homosapiens, which are useful for explanation and prediction in biology—or, indeed, any other science.5 Two things about these reasons for scientific eliminativism are worth emphasising. First, and again, the reasoning is explicitly pragmatic.6 References to memory as such (as against memory types) should be eliminated from scientific generalisations if explanatory and predictive utility is thereby increased. References to human races should be eliminated from scientific generalisations if utility is thereby increased. Second, notice that adopting scientific eliminativism isn’t antagonistic to scientific inquiry; rather, it is an appropriate part of scientific progress. Progress in science not only involves increasingly successful explanations and predictions about the members of a kind but crucially also involves discovering that some of the kinds of things that we had been offering scientific generalisation about are not usefully generalised about after all—at least not for scientific explanations and predictions. We perhaps do better to offer scientific generalisations about memory types than memory and to offer scientific generalisations about homosapiens than any of the human races. Discovering these things, and adopting the corresponding scientific eliminativism for memory as such and for human races, would not hinder scientific progress—it would constitute it. We can now ask the central question of the present chapter this way: should we be scientific eliminativists about pain, pain types, both, or neither? Recall that some philosophers take natural kinds to be all and only those which are subject to mechanistic explanation, and yet others to require of mental kinds, in particular, that they must in principle be subject to mechanistic explanation. If we follow these philosophers, then we already have an argument for scientific eliminativism for both pain and pain types. If we think, that is, that science only appropriately generalises about (at least mental) kinds which are explained, or determined, by the workings of a mechanism, then the conclusions of the previous chapter are enough to show that science doesn’t appropriately generalise about pain or pain types. References to these should then be eliminated from science.

146  Adopting Scientific Eliminativism Our more liberal scientific utility criterion for natural kinds, however, allows that science may sometimes offer useful generalisations about kinds which are not mechanistically explicable. For purposes here, as introductorily noted, we are going to grant that lacking a mechanistic explanation is a strong, but nonetheless inconclusive, reason to think that a kind is not natural. We’ll grant that if a kind can’t be mechanistically explained—not just not yet, but in principle—that’s a good reason to think that it’s a kind that’s not useful for scientific explanation and prediction. Indeed, following some of the last century’s leading philosophers of mind, let’s grant that this may be a particularly strong reason when we are considering whether a posited mental kind is a natural kind. Again, though, we’ll also allow that this strong reason is not conclusive.7 Contrary to these philosophers, perhaps pain and pain types are natural kinds, even if they aren’t mechanistically explicable. Using this more liberal criterion for natural kinds, scientific eliminativism for pain or pain types won’t simply follow from the previous chapters. To consider the possibility that pain satisfies the scientific utility criterion, despite the mechanistic differences between token pains revealed through scientific inquiry, it’s helpful to introduce the final technical notion of this chapter: pluralism. I’ll define pluralism about a kind as the claim that, despite mechanistic differences across the kind’s members, the kind is nonetheless usefully referenced in (at least some) generalisations of (at least one) science. To be a pluralists about pain or pain types is to hold that, despite their mechanistic differences, it is useful for science to offer (at least some) generalisations about pain or pain types for explanation and prediction. Pluralism will often be plausible because mechanistic differences between the members of a kind are often relevant for some scientific generalisations, but negligible for others. As an everyday example: you might have the same application on your phone and on your computer, e.g. Skype. There will be differences in the mechanistic activity which determines the functioning of that application on your phone and on your computer. Nonetheless, for many purposes, those differences are negligible for generalisations which may be usefully offered about the application and its functioning. We can use (at least some) generalisations, which ignore the mechanistic differences, to explain and predict the workings of the application on both your phone and computer. We can, for instance, predict what will happen when you click on a certain icon or explain why something happened when you clicked on another. Of course, there will be some things about the functioning of the application on your phone and computer, respectively, which we will only be able to explain or predict by talking about the mechanisms which differ between them. For a more specialised, scientific example: some differences in the chemical compositions of the molecules in a lake may be

Adopting Scientific Eliminativism  147 irrelevant for the success of some explanations and predictions offered by, e.g., limnology (i.e. the study of inland aquatic ecosystems), even though these same differences will be crucial to the success of some explanations and predictions about those molecules offered by, e.g., chemistry. Similar examples proliferate. These examples evidence that mechanistic differences which are crucial for some scientific explanations and predictions are negligible for others, such that it is sometimes useful to generalisation about a type despite the mechanistic differences across its tokens. When we consider that there are a wide range of scientific inquiries, with distinct explanatory and predictive purposes, we can see that there will be a profundity of kinds about which we should be pluralists.8 We can now ask the central question of the present chapter in the final, following way: should we be scientific eliminativists or pluralists about pain, pain types, both, or neither? As the discussion above hopefully makes clear, to answer this question we must consider the utility of the references to pain and pain types within the generalisations of the relevant sciences. Are references to pain or pain types useful for the explanations and predictions at which those generalisations aim? Are there useful scientific generalisations that we would lose by eliminating these references? If the answer to these questions is yes, then we should be pluralists. We should retain those references and accept the naturalness of the kinds, despite their mechanistic differences revealed in the previous chapter. If the answer is no, however, then we should be scientific eliminativists. However heterodox such scientific eliminativism may be. Upon initial reflection, we might think it obvious that we should be pluralists. Upon initial reflection, that is, we might think it obvious that we should retain references to pain and pain types for scientific inquiry. Grouping particular pains, which seem obviously to exist, into both types and the overall grouping of pain as such may seem obviously useful for a wide range of scientific inquiries. As merely glimpsed in the previous chapters, pain science is burgeoning. The revolution in pain science, begun with Melzack and Wall’s gate-control theory, has led to an explosion of new theories, models, treatment interventions, and experimental paradigms. Surely references to pain and pain types, within the flourishing vistas of pain science, are bearing fruit. Neuroscience, psychology, biology, and more besides all generalise about pain and pain types, and these generalisations are apparently useful for explaining and predicting particular token pains. After all, we might think our explanations and predictions about pains are a lot better now than they used to be, as evidenced by the fact that treatment for pain is apparently better now than it used to be. Progress in our understanding of pain is being made. To continue making that progress—we might think it obvious—requires us

148  Adopting Scientific Eliminativism to continue to generalise about both pain types and pain as such, and to submit these to further scientific inquiry. Similarly, for those with a naturalistic, physicalist bent like me, it is admittedly downright unintuitive to hold that pain or pain types aren’t appropriate objects of scientific inquiry about which we may usefully generalise. Surely, I initially assumed, we can have a robust, useful, and legitimate pain science focussed on pain and pain types—however complex and idiosyncratic each token pain may be. The goal in taking complex idiosyncrasy seriously is to improve pain science, not to undermine it! Insofar as pluralism allows for some mechanistic differences across tokens, it initially looked to me to provide a promisingly plausible way to avoid scientific eliminativism, while still accepting the complex idiosyncrasy that pain science has revealed. In this chapter, however, I argue for scientific eliminativism for both pain and pain types. References to these kinds—surprisingly, to my mind—are not useful for explanation and prediction when occurring in scientific generalisations. Ultimately, the reason for this turns out to be what we’ve already seen: the idiosyncratic convergence of the activity of multiple mechanisms which determines each token pain. The idiosyncrasies of this complex convergence are not negligible for successful explanation and prediction when referenced in scientific generalisations. Moreover and crucially, however, references to the mechanisms which are implicated in some token pains but not others are usefully generalised about for scientific explanation and prediction. It is discoveries and successful generalisations about these implicated mechanisms which explains the flourishing of pain science. Accordingly, the core proposal of this chapter is that no scientific utility is lost by eliminating references to pain or pain types, as long as references to implicated mechanisms are retained. I proceed as follows. The following section contains the arguments that we should reject pluralism in favour of scientific eliminativism. We’ll directly consider the explanatory and predictive utility of generalisations which refer to pain and pain types. In particular, we’ll consider whether retaining generalisations which refer to these are explanatorily and predictively useful for any scientific inquiry, over and above retaining generalisations which refer to mechanisms implicated in pain tokens. I’ll argue that it isn’t. In Section 4.3, I consider two objections. First, that the widely accepted International Association for the Study of Pain (IASP) definition of pain identifies a referent which is usefully referenced in scientific generalisations. I argue that it doesn’t. Second, that the ­progress of pain science evidences the utility of references to pain and pain types. I argue that it doesn’t. In Section 4.4, I conclude with some worries which the preceding sections and chapters may have raised about pain outwith scientific inquiry. These lingering worries will take us to the final two chapters.

Adopting Scientific Eliminativism  149

4.2 Rejecting Pluralism I now argue against pluralism, and in favour of scientific eliminativism, for both pain types and pain as such. The reasoning here is explicitly pragmatic: explanation and prediction, the aim of scientific generalisations, is more successful when we eliminate these references. So long, as we’ll see, that references to the mechanisms implicated in token pain experiences are retained. Consider first, pain as such. Are references to pain as such in scientific generalisations useful despite the mechanistic differences across token pains revealed in the previous chapters? If so, we should adopt pluralism for pain. If not, then we should reject pluralism in favour of scientific eliminativism. How might we go about answering this question? One thing that we obviously can’t do is to consider, one by one, all of the scientific generalisations about pain which are currently on offer. What we can do, however, is to consider some generalisations schemas for pain. These schemas are rough and ready models of scientific generalisations about pain. I deploy them to illuminate why any particular scientific generalisations about pain actually on offer will be more useful for explanation and prediction if the references to pain as such are eliminated.9 Accordingly, consider the following three generalisation schemas for pain: G1: Pain is caused by _____. G2: Pain is relieved by _____. G3: Pain causes _____. My claim is that whatever we put in these blanks, the generalisation will facilitate more successful scientific explanations and predictions— including, especially, explanations and predictions of token pains—if the references to pain as such are eliminated in favour of references to mechanisms. There are, that is, no useful scientific generalisations that would be lost by eliminating the term ‘pain’ from further scientific inquiry. This may admittedly initially strike the reader, as it struck me, as highly unintuitive. It initially seems as if G1–G3 can be easily completed in many ways which are useful for the explanations and predictions at which offered scientific generalisations aim. We may, for instance, complete G1 with ‘getting hit on the head’. This seems to be an unproblematic, common piece of our everyday wisdom about pain. Consider, however: how reliable is this generalisation? What explanations and predictions, for what science, does it facilitate? I submit that it is not adequate for any scientific generalisations. To see this, notice that it will, after all, be false when the hit on the head is

150  Adopting Scientific Eliminativism slight. And, crucially, what counts as a slight hit on the head is highly idiosyncratic; whether hits on the head cause pain will vary from person to person and from circumstance to circumstance. As we’ll see in more detail in the following chapter, the difficulties for the explanatory and predictive utility of this candidate generalisation are everyday difficulties caused by the everyday variation that we routinely take for granted, and for which we adjust, in our everyday lives. The point for present purposes, however, is that this everyday idiosyncrasy in the causes of pain as such undermines the utility of generalisations about pain as such for scientific inquiry. As a piece of everyday wisdom, ‘pain is caused by getting hit on the head’ may be useful. For any scientific inquiry, it is not. To make this point perhaps most forcefully, recall that treatment is the crucible for the theories of pain science. Treatment is the central goal of pain science: it is treatment, above all, for which we want our scientific generalisations about pain to be useful. If we try to complete any of G1–G3 such that the candidate generalisation is adequate for treatment purposes, we fail miserably. Consider the candidate completion of G2 with ‘morphine’. This, too, initially seems plausible: we might confidently offer the generalisation that pain is relieved by morphine. And this may initially seem useful even for treatment purposes. Unfortunately, however, it is problematic. Consider first that the amount of morphine is crucial for any kind of relief: too little and the pain remains—as unpleasant as ever—but too much and the pained person dies. Crucially, notice now that the amount of needed morphine—a key quotient for treatment purposes—is highly idiosyncratic.10 Going further, however, one core difficulty we’ve already seen in the previous chapter is that morphine lacks validity as a treatment intervention for pain as such; like being knocked out cold to eliminate pain, taking morphine knocks out wide swaths of functioning. At the same time, a further core difficulty with the explanatory and predictive adequacy of the candidate generalisation is that the unpleasantness of some token pains is left untouched by morphine, such that sufferers get no relief.11 Yet further, as we saw in Chapter 2, there is reason to doubt whether morphine ever relieves pain as against merely relieving the unpleasantness of pain; people receiving morphine typically continue to report pain—pains whose affect has been altered (and again, sometimes, not even that). ‘Morphine’ is, to my mind, one of the most plausible candidate completions of G2. The inadequacies of other contenders, e.g. ‘aspirin’, ‘a good night’s sleep’, ‘antacids’, or ‘a glass of water’, are all even more woefully inadequate for scientific explanation or prediction. If we use treatment as the crucible for testing the utility of generalisations about pain as such, then any candidate completion of the schemas above will have clear inadequacies.

Adopting Scientific Eliminativism  151 Even if candidate completions of the above schemas suffer from inadequacies, however, one might demur from elimination. Aren’t scientific generalisations about pain as such aimed at explaining and predicting pain as such? And how in the world, one might wonder, will those explanations and predictions be improved by eliminating all references to pain? “Pain is caused by getting hit on the head”, however unreliable or inadequate for scientific inquiry or treatment purposes, has at least some reliability. If we eliminate all references to pain as such, aren’t we left without any explanatory resources? Isn’t that less utility than we would have by retaining the references to pain? Similar considerations apply, and perhaps with more force, when we turn to treatment purposes. “Pain is relieved by morphine” is surely more explanatorily and predictively useful than nothing. At least referring to pain as such gives us some explanatory and predictive power—however inadequate the generalisations which refer to pain as such may be. This is an important concern. In response, I make two replies that also further clarify what scientific eliminativism for pain does and doesn’t involve. First, it is the very scientific utility of the kind—pain as such—that we are attempting to consider. While we might have expected pain science to appropriately aim at explaining and predicting pain as such, it may turn out that token pains are better explained by ceasing to group all token pains together in this kind. Indeed, to take eliminativism for pain as such seriously is to take seriously that this sort of taxonomic error may well have occurred. Recall our introductory discussion of memory. Memory is a posit of our everyday theory of ourselves. But, as above, it may be that we would do better, for scientific inquiry, to generalise only about memory types as against memory as such. When would this be so? When elimination of references to memory as such would allow us to better explain and predict the instances of memory for which we want our generalisations to facilitate successful explanations and predictions. If we can better explain and predict token pains by eliminating references to pain as such, then that is what we should do. The suggestion is that the kind or grouping—pain as such—is one that actually gets in the way of what we want our pain science to be able to explain and predict—namely, token pains. Scientific eliminativism for pain as such involves ceasing to take pain as an appropriate kind, or grouping, for scientific inquiry. If we eliminate references to pain as such, then we won’t offer adequate explanations and predictions of it, even as we might cease to offer adequate explanations and predictions of memory as such as against types of memory. If elimination of references to pain as such is justified, it is on the grounds that we would thus be able to offer better explanations and predictions of particular token pains. Second and crucially, pain as such is not the only potential referent on offer for the scientific generalisations which may facilitate explanation

152  Adopting Scientific Eliminativism and prediction of token pains. It is not pain as such or nothing. In particular, we may retain the many generalisations about the many mechanisms discovered to be implicated in pain tokens through research into pain as such. Not only is there no need to eliminate references to these mechanisms from our scientific generalisations, there is every pragmatic reason to retain them. Generalisations about pain as such are undermined by the idiosyncrasy of the convergent activity of these mechanisms which explains, or determines, each particular pain. But it is crucial that we retain the generalisations about those mechanisms which, we have discovered, may (but may not) be implicated in any particular pain. Scientific eliminativism for pain as such does not involve ceasing to offer any scientific generalisation relevant to explaining or predicting token pains. In particular, as I now stress, it does not require eliminating references to any mechanisms. The core idea is that by eliminating references to pain, but retaining references to mechanisms (e.g. those discovered by previous inquiries into pain), the resultant generalisations will yield explanations and predictions which are more successful. Recognising treatment as the crucible for theory can perhaps facilitate our seeing this most clearly. To return to G2, for example, rather than offer the generalisation that ‘Pain is relieved by morphine’, we do better to offer generalisations concerning the mechanistic activity which is targeted by morphine, e.g. broadly, the release of certain neurotransmitters.12 Generalisations about the relevant mechanisms and activities will be more useful for explaining and predicting both morphine and any token pains in which the release of the relevant neurotransmitters is likely to be a key convergent mechanism. These generalisations will, that is, be more useful—among other things—for the treatment of token pains. The goal of pain science is treatment, and for this laudable goal we do best to eliminate references to pain as such, while retaining references to those mechanisms which may be implicated on the particular occasion of the token pain of the person we are seeking to treat. With the above points in mind, consider now G3. Again, adequate completion initially seems easy. For everyday purposes, we apparently find it easy to fill in the blank with a myriad of everyday behaviours which we take to be caused by pain. She cried because she was in pain. I was distracted because of the pain. We often offer these kinds of everyday explanatory generalisations of our own and others’ behaviours. Consider thus the candidate completions of G3 with, e.g., ‘crying’ or ‘distraction’. Are these or any other similar candidates from our everyday theory adequate for scientific generalisations? I submit that they are not. Whether a pain causes crying or distracting depends on a number of highly complex, idiosyncratic features of the pain and the pained. As when considering G1, notice that we routinely take these everyday idiosyncrasies into account in our everyday explanations and predictions.

Adopting Scientific Eliminativism  153 But as there, and when considering G2, these idiosyncrasies nonetheless undermine the success of the generalisations for pain science. Candidate completions of G3 would be more successful for any scientific inquiry if we replaced references to pain as such with references to relevant mechanisms, sometimes implicated in token pains. To further clarify these points, consider in more detail the candidate completion: ‘Pain causes distraction’. This generalisation is less explanatorily and predictively useful for any science than the generalisations attained by referring instead to mechanisms—sometimes converging to contribute to the determination of a token pain—which have been discovered to cause distraction or draw attention. In seeming contradiction to this, note that in a much-cited article, Eccleston and Crombez (1999) offer a model of the way in which ‘pain demands attention’. In attending to the model, however, it becomes clear that it is, roughly, threat and intense sensations (along with a suite of environmental variables) which determine whether and to what degree any token pain demands attention. Any seeming success of the generalisations about pain is a consequence of the activity of threat detection mechanisms and the processing of intense sensory stimulation. As we have seen in the previous chapters, however, some pains involve threat detection and intense sensory simulation, but much threat detection and intense sensory stimulation occur in the absence of pain. (Orgasms, for instance, demand attention, as does a robber shouting ‘your money or your life’.) And as we’ve seen (and as is indeed common sense), some pains are neither threatening nor involving intense sensations. The candidate generalisations will fail in these cases. The utility of the scientific generalisations gleaned from Eccleston and Crombez will, however, increase if we eliminate references to pain as such, and retain references to threat detection mechanisms and intense sensory stimulation processing. Despite the important work and the popularity of this article, it is apparently not pain as such which demands attention, but threat and intense sensation. Examples proliferate. Though candidate completions of schemas G1– G3 are offered in contemporary pain science, I submit that the utility of the generalisations will increase if references to pain as such are eliminated, while references to the mechanism discovered to be implicated in some (but, as we’ve learned, not all) token pains are retained. The point isn’t that it is never useful to group the activity of mechanisms together into a more complex mechanism. Threat detection mechanisms, for instance, are themselves complex. The crucial point is instead that no utility for scientific explanation and prediction would be lost by eliminating references to pain, so long as we retained references to these other mechanisms; rather, some would be gained. The moral is that the mechanistic differences between token pains are not negligible to scientific generalisations about pain as such. Because each token pain is caused by the idiosyncratic convergence of multiple

154  Adopting Scientific Eliminativism mechanisms, the utility of scientific generalisations increases when we eliminate references to pain as such and retain references to the mechanisms implicated in pains. For pain as such, pluralism is thus to be rejected in favour of scientific eliminativism. Turn now to pain types. Consider the same key question: are references to pain types in scientific generalisations useful despite the mechanistic differences across token pains revealed in the previous chapters? If so, we should adopt pluralism for pain types. If not, then we should reject it in favour of scientific eliminativism. As with pain as such, utility favours rejecting pluralism and eliminating references to pain types from scientific generalisations. And for the same reasons. While we again cannot consider every scientific generalisation referring to pain types which is currently on offer, consider the following four generalisation schemas: G4: Inflammatory pain is caused by _____. G5: Inflammatory pain is relieved by _____. G6: _____ is a reliable intervention for chronic pain. G7: _____ is a reliable intervention for headaches. Of these, first briefly consider whether their candidate completions are more useful for scientific explanations and predictions than candidate completions for G1–G3. It seems to me that at least some candidate generalisations for pain types are apparently more explanatorily and predictively useful than those for pain as such. Consider, for instance, G5 and the candidate completion of ‘aspirin’ as against this candidate completion for G2. The former is apparently more useful—well known by marketers of aspirin who develop commercials focussed on headaches and not paper cuts. We should, indeed, perhaps have expected that generalisations about these are more scientifically useful than those about pain as such—at least for some pain types. Pain types, recall from the previous chapter, are most often constructed by etiology or symptoms. While we saw that these are not well-correlated with the functioning of any mechanism, there is nonetheless presumably a narrower range of mechanisms implicated in the tokens of at least some of these pain types than the general grouping of pain as such. As a result, it is then to be expected that generalisation about inflammatory pain, for instance, will be more useful for explaining and predicting tokens of inflammatory pain than generalisations about pain as such will be for explaining and predicting tokens of pain as such. This may sound a bit complicated, but the idea is the simple one that fewer mechanisms are implicated as potential contributors to the idiosyncratic convergence which determines a token of, e.g., inflammatory pain, in particular, than a token pain, in general.

Adopting Scientific Eliminativism  155 For some pain types, however, it may be that the range of potentially implicated mechanisms is no narrower. Chronic pain, for instance, may be such a pain type. While multiple idiosyncratically converging mechanisms determine the tokens of every type of pain, some pain types may include a narrower range of implicated mechanisms than pain as such. If so, then generalisations about these pain types will presumably be more useful than generalisations about pain as such. Generalisations about pain types which do not narrow the range of mechanisms which may be implicated in any token instance, however, will be no more useful for the explanations and predictions at which they aim than those concerning pain as such. The narrower range of implicated mechanisms explains why some pain types are more usefully referenced in scientific generalisations than others or than pain as such. We may put this point a bit more technically by saying that some pain types are more natural than others and more natural than pain as such. Groupings of token pains into types have variable utility when referenced in scientific generalisations. Put thus bluntly, it is again what we should expect. It would be rather surprising if any old grouping of token pains into types was as useful for explanation and prediction as any other. About even the most natural pain types, however, I submit that pluralism should be rejected in favour of eliminativism for precisely the same reasons pluralism for pain as such is to be rejected: each token of not only pain as such but of each pain type is determined by the idiosyncratic convergence of the activity of multiple mechanisms, and the idiosyncrasy of this convergence is not negligible to the explanatory or predictive utility of the generalisations about the pain type. The differences between your inflammatory pain yesterday and my inflammatory pain today are relevant to the success of any scientific generalisations we may offer about inflammatory pain. As with pain as such, we should eliminate references to pain types from our sciences—as long as references to implicated mechanisms are retained. Consider again G5 and inflammatory pain. No useful generalisations would be lost if we eliminate references to inflammatory pain, as long as we retained references to inflammatory mechanisms—many of which, indeed, were discovered in pursuit of a mechanistic explanation of inflammatory pain. As with the generalisations concerning pain as such considered above, the seeming success of generalisations referring to inflammatory pain depends on the oft-implicated inflammatory mechanisms. No utility would be lost, and some would be gained, if we eliminated the reference to inflammatory pain in the temping candidate completion of G5, and retained those scientific generalisation which referred instead to inflammatory mechanisms. These retained generalisations would include, for instance, those which capture the ways in which they are affected by nonsteroidal anti-inflammatory drugs (NSAIDs)

156  Adopting Scientific Eliminativism like aspirin. Our generalisations about the workings of inflammatory mechanisms are useful and reliable—but we are well aware that no one of these particular inflammatory mechanisms determine or explain inflammatory pain. This is why, as most of us who have suffered it know, though inflammatory pain is often relieved by aspirin, it sometimes is not. Other mechanisms also contribute to the determination of every token inflammatory pain. The points generalise. Even as eliminating references to more natural pain types, e.g. inflammatory pain, does not decrease utility, so eliminating references to even less natural types does not decrease utility. As long as generalisations concerning those mechanisms implicated in tokens of the type are retained, utility will increase. Examples again proliferate. Generalisations about pain types are still readily offered in contemporary pain science. These are, if anything, more prevalent than offered generalisations about pain as such. The same morals, however, apply. Blom et al. (2014), for one example among many, offer an article entitled ‘Nerve injury-induced neuropathic pain causes disinhibition of the anterior cingulate cortex’. Upon careful inspection, it’s clear that Blom et al.’s results show that peripheral nerve damage can cause cortical disinhibition. But as we—including Blom and colleagues—know, not all peripheral nerve damage results in neuropathic pain, nor is neuropathic pain well-correlated with peripheral nerve damage. As Blom themselves note even in the abstract (emphasis added): “These changes at the cortical network level might therefore contribute to the neuropathic pain condition”. As ever, the particular discovered mechanism will not determine or explain any token pain apart from the idiosyncratic convergent activity of others. Similar considerations apply to all examples from the literature which I can find. As when considering pain as such, the point isn’t that it is never useful to group the activity of mechanisms together into a more complex mechanism. The crucial point is instead that no utility for scientific explanation and prediction would be lost by eliminating references to pain types, so long as we retained references to these other mechanisms; rather, some would be gained. Again, I thus submit that the utility of the generalisations will increase if references to pain types are eliminated, while references to the mechanism discovered to be implicated in some (but, as we’ve learned, not all) token pains are retained. Multiple mechanisms are implicated as potentially converging to explain any token pain of any pain type. The idiosyncrasy of this mechanistic convergence is not negligible to the scientific generalisations we may offer that refer to groupings of any tokens into types. We should eliminate references to these types in our scientific generalisations, and retain references to the mechanisms implicated in the tokens. We should, that is, reject pluralism for pain types in favour of scientific eliminativism.

Adopting Scientific Eliminativism  157 Again, one may worry: if we eliminate references to pain types from our scientific generalisations, then surely we can’t better explain or predict those pain types. Again, I answer: these groupings of token pains are not useful for explaining or predicting them; rather, we do better to deploy generalisations about those mechanisms which may be implicated in each token pain. The very question of whether we should be scientific eliminativists or pluralists about pain types is the question of whether the groupings of token pains into these types is useful. If the arguments above are correct, then it isn’t. As an analogy, remember the silly type, Postuff. It is true that if we eliminate all references to Postuff from our scientific generalisations, then we’ll be left without any scientific generalisations for explaining or predicting Postuff. Nonetheless, if we eliminate references to Postuff, but retain references to potted plants, politicians, and potatoes we will be able to better explain and predict all instances of those. Lumping those together into one group is, we presume, not useful for any scientific inquiry. So too, I am arguing that lumping together token pains into types, or into the overall grouping of pain as such, is not useful for any scientific inquiry. This is, of course, a more surprising claim for pain and pain types than the silly type, Postuff. If the arguments above are correct, however, then the reasons to be scientific eliminativists about pain and pain types are the same as the reasons to be scientific eliminativists about Postuff: references to the grouping in scientific generalisations are not useful for the explanations and predictions at which those generalisations aim. I conclude that we should reject pluralism, in favour of scientific eliminativism, for both pain types and pain as such. Our explanations and predictions of pain, including and especially for treatment, will improve if we cease to group token pains into kinds and offer generalisations about those groupings, i.e. pain types or pain as such. Rather, we should retain generalisations concerning the workings of the mechanisms discovered to be implicated in some token pains, but—we have also discovered—not in others. Neither pain nor any type of pain is usefully referenced in scientific generalisations. In closing this section, briefly consider the implications of this scientific eliminativism for the status of pain science. Science trucks in generalisations. In doing so, it trucks in types and not tokens. Scientific inquiry isn’t aimed at uncovering the determinations or providing explanations of particular token pains. Indeed, as far as I can tell, no science is interested in the particular tokens of anything.13 Instead, science offers generalisations about types of things, with the aim of explaining and predicting the tokens of those types. Concerning pain: scientific inquiry necessarily glosses over individual differences to offer generalisations about pathways, brain activity, or any other type of thing which is under investigation. Adequate explanations of each token pain, however,

158  Adopting Scientific Eliminativism crucially rely on these individual differences and their idiosyncratic convergence. As seen in the previous chapter, the explanatory determinates of each token pain include the genetic, molecular, chemical, biological, and social factors relevant to a particular individual’s pain at a particular time. These differences are not negligible to the candidate generalisations about pain or pain types which scientific inquiry may offer. The dilemma for pain science, then, is that while adequate explanations of each token pain are individualised explanations, science is not in the business of offering individualised explanations. Adequate explanations of each token pain are idiosyncratic, but scientific inquiry is general. How, then, can we have a science of pain? This concern is perhaps most stark when we turn yet again to treatment. As Woolf and various collaborators emphasised numerous times (1998, 1999, 2001): the difficulty of recognising the highly idiosyncratic nature of token pain experiences in the clinic is exacerbated by the fact that pain research almost always glosses over individual differences, for instance, in drug trials and neuroimaging. This is not only a theoretical problem for generalisations about pain as such or pain types, but a practical problem in the clinic where theories are tested. For treatment purposes, the failure to recognise relevant individual variability has detrimental practical consequences. As discussed in the last chapter, however, the mechanism-based approach advocated by Woolf and collaborators didn’t resolve the difficulty for pain science. Moving to mechanism-based classification didn’t and won’t yield adequately individualised explanations because the convergence of the mechanistic activity is itself idiosyncratic. The dilemma for pain science is that scientific generalisations inevitably abstract away from individual differences, but those differences are crucial determinates of each token pain experience. This is seen clearly when we continue to take treatment as the crucible for theory: recognising individual differences, and the crucial role that they play is essential to the effective treatment of the individual token pains presented and requiring treatment in the clinic. Any science of pain which ignores these individual differences is thus inadequate. But in offering scientific generalisations, it seems that the science of pain must inevitably abstract away from these individual differences. The surprising heterodox conclusion is that pluralism for pain and pain types should be rejected in favour of scientific eliminativism. While our generalisations about mechanisms are explanatorily and predictively useful, each token pain is determined by the idiosyncratic convergence of mechanistic activity. The idiosyncrasy of this convergence is not negligible for the explanatory and predictive utility of the generalisations about the groupings of token pains we may construct into pain types or the overall type pain as such. The differences between our pains matter. To better explain and predict pain, we need to take its complex idiosyncrasy

Adopting Scientific Eliminativism  159 seriously. While we should retain references to implicated mechanisms in our scientific inquiries, references to pain and pain types should be eliminated. To be clear: more and more mechanisms implicated in pain are being discovered all the time. These discoveries yield novel treatment targets. I expect that this will continue and that we will uncover additional mechanisms about which we can usefully generalise and which we may sometimes appropriately target for treatment. We will undoubtedly come to better understand, for some few instances, how the different systems of the body interact, how different receptors are facilitated or inhibited, and much more. It is useful and important research, among other things, for explaining and predicting token pains. The role that any one implicated mechanism plays in a token pain, however, is also determined by the activities in numerous other relevant mechanisms. Each token pain is partially determined by an individual’s particular genetics, chemistry, biology, memories, upbringing, culture, and much else that we are still trying to understand. The convergence of this mechanistic activity is idiosyncratic to such an extent that generalisations about pain types or pain are not useful for scientific inquiry—though generalisations about the mechanisms we are discovering to be potentially implicated certainly are. Strictly speaking, then, pain is not an appropriate object of scientific inquiry, though the mechanisms implicated in pain are. For pain as such and for pain types, we should reject pluralism and adopt scientific eliminativism. We should continue to use scientific methods to investigate the mechanisms implicated in token pains. We may well, and should, continue to use the fruits of these investigations to develop novel treatments and interventions—some of which will be appropriate in response to particular pain reports. Accordingly, we may even, if we like, continue to refer to these investigations as pain science. But even as the conclusion of the previous chapter was that we should not seek mechanistic explanations of pain or pain types, so we should not seek scientific generalisations about pain or pain types. And for the same reason: the idiosyncratic convergence of mechanistic activity which determines each token pain undermines both mechanistic explanations (as argued in the previous chapter) and the utility of scientific generalisations referring to pain or pain types (as argued above). Pain science can do better. If pain science should eliminate references to pain and pain types, should we also eliminate such references in everyday life? Before turning to this question in the next chapter, I address two powerful objections.

4.3 Objections The argument for scientific eliminativism for pain and pain types rests on the deliverances of pain science itself. Pain is a posit of our everyday

160  Adopting Scientific Eliminativism theory of ourselves, and we have submitted that posit to scientific inquiry. It was those inquiries which revealed the complex idiosyncrasy of pain which undermines the scientific utility of reference to pain or pain types. The idea that pain science itself has delivered revelations which undermine its offered generalisations may prompt concerns. After all, how have pain scientists, and indeed clinicians, been dealing with the complex idiosyncrasy of pain? It’s not by adopting scientific eliminativism! As a cursory glimpse through any pain science journal will reveal, pain science is flourishing. This prompts an important objection: doesn’t this flourishing show that references to pain and pain types are useful, such that something must be wrong with the above arguments? Indeed, far from adopting scientific eliminativism, having grappled with the complex idiosyncrasy of pain, pain scientists and clinicians together formed the IASP and offered a definition of ‘pain’. This prompts another objection: doesn’t the IASP definition identify a referent usefully retained for scientific generalisations? In this section, I respond to these two objections. I first consider the IASP definition of pain. I argue that it does not identify a referent useful for scientific inquiry, was not intended for this purpose, and is anyway problematic for use in the clinic or everyday life. Turning to the flourishing of pain science, I argue that pain science has flourished despite references to pain as such or to pain types and not because of them. Scientific eliminativism for pain and pain types is best understood as constituting progress in pain science. 4.3.1 The IASP Definition of ‘Pain’ The IASP published its first definitions of pain terms in 1979. Notice that this offering comes about 15 years after the introduction of gate-control theory, as pain science was beginning to undergo revolution. As seen in the previous chapter, specificity and intensity theories were being rejected in favour of convergent, multidimensional models. A task force comprised of prominent pain scientists was commissioned to develop definitions of pain terms which reflected the budding revolution. The definitions have subsequently been reviewed multiple times in committee, with the most recent review in 2011. Numerous researchers, including Patrick Wall, of gate-control fame have contributed to these definitions. The editor and final arbiter, however, has always been Harold Merskey. Only minor revisions have ever been made to the original definition of ‘pain’, and it continues to be widely accepted as authoritative. It is offered, at least in passing, in a profundity of articles and studies on pain. It is adopted by leading clinical bodies of pain research beyond the IASP, e.g. the World Health Organisation. Though not entirely without

Adopting Scientific Eliminativism  161 detractors, it is difficult to overstate the extent of its reach and the degree to which it receives at least lip service. The definition currently reads: “An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage”.14 The lengthy appended note, clarifying the definition, has received at least as much attention in the literature as the definition itself. It reads: 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. Note a few initial things about this definition and lengthy note. Both sensation and emotion are explicitly included as components of pain and said to be associated, but only associated, with tissue damage. Pain is also explicitly defined subjectively. The definition also builds in that a person is incorrigible (i.e. cannot be corrected) about whether they are in pain: if pain is sincerely reported, then pain should be accepted as occurring—whatever further examination might reveal. It is also claimed to be always unpleasant.15 Moreover, especially in its last sentence, the definition implies a contrast between the physical and the psychological altogether. Lacking any biological marker for pain, the IASP’s definition groups all token pains into one type by focussing on the supposed psychological aspect alone. There is no identification here of any

162  Adopting Scientific Eliminativism of the mechanistic determinants of pain or, indeed, anything observable which might allow us to explain or predict pain whatsoever. Tissue damage is only ‘usually associated’ with the pain experience—and, indeed, potential tissue damage is here taken to be just as associated with this experience as actual tissue damage. According to the IASP, pain is never constituted by a physical process, is always psychological and subjective, and only sometimes has a physical cause. The IASP definition does not identify anything usefully referenced for scientific generalisations. One way to begin to see this is to consider the ways in which the definition has been defended and advocated by the scientists and clinicians who have offered it. Consider, for instance, the way in which Harold Merskey and Patrick Wall defend the definition from a challenge by Kanwaljeet Anand and A.D. Craig (1996a). The latter attack the definition on the grounds that it inappropriately rules out attribution of pain to all non-verbal creatures. This is a version of an objection that philosophers sometimes refer to as the ‘children and animals’ objection to various characterisations of mental episodes. A characterisation of a mental episode is subject to this objection when it, apparently illegitimately, fails to extend to young children and non-human animals. While I think there are a number of ways that advocates of the IASP definition may effectively respond to this challenge, the way that advocates in fact responded is illuminating for present purposes. Merskey (1996, p. 209), in reply, claimed that the definition is not intended to be “… a statement of absolute truth but a statement of the way in which we employ a term”. Note that the relevant ‘we’ is not the pain scientist, but the everyday person using the term in everyday life. He admits, as perhaps he needn’t, that the definition has contributed to inadequate care of infants and other pre- or non-verbal humans. He claims, however, that this is not a problem with the definition. Rather, the definition is correct if it accurately reflects common usage: that is all the definition is intended to do. It is worth emphasising the way in which Merskey explicitly distances the referent of ‘pain’ from everyday usage he takes the IASP definition to have identified and any proper objects of treatment. Treatment should focus on particular behaviours, neural activity, or other observables. But he explicitly holds that none of these are, at least at the time of his writing, well-correlated with the referent of pain as referenced through common usage of the term ‘pain’. We should attempt to treat, and research, those things we can observe, but the everyday referent of pain does not identify any such thing. Common usage is not thereby altered— nor should we ‘misuse our energy’ in attempting to alter common usage to suit our treatment aims. The goal of the task force is to make common usage explicit—and he believes the offered definition accurately does

Adopting Scientific Eliminativism  163 this, though it does not identify anything which is well-correlated with anything observable, any physical process, or a treatment target. Merskey is the head of the IASP task force offering the definition of pain. According to him, it is a definition which seeks—and he thinks succeeds—in identifying the referent of ‘pain’ as deployed in our everyday life as part of common usage. There is no suggestion here that the IASP definition identifies something which may be usefully referenced in scientific generalisations. Indeed, all the suggestions about the nature of the everyday referent are to the contrary. Wall’s own (1996) similar, brief response to the challenge presented by Anand and Craig is likewise instructive. For treatment purposes, he decries the very question ‘Is this organism in pain’ in favour of the question ‘Would you interfere with the integrity of an organism’. The response highlights that Wall, at least, thinks these are very different questions. For an intervention, there are anatomical, biological, and behavioural considerations. Wall believes that none of these correspond well to the referent of ‘pain’ as this word is commonly deployed in our everyday lives. Accordingly, whether an organism is in pain is not a useful question for whether to take action or for illuminating what kind of action should be taken. Like Merskey, Wall accepts the IASP definition as capturing our everyday notion of pain, and thus maintains that a sincere report of pain tells you whether the person is in pain. But that, according to Wall, tells you nothing about the state of the organism which may be useful for treatment. As already noted in Chapter 1: according to Wall, the binary question—pain or no—is diagnostically inert. There is again no suggestion here that the IASP definition identifies something which may be usefully referenced for scientific generalisations—all suggestions about the nature of the everyday referent are to the contrary. In further considering the intended aim of the IASP definition, consider the oft-ignored preamble offered by the task force. The definition is introduced with the note that it is not intended as a “constraint on further developments” and that “[i]t is important to emphasise… that the terms have been developed for use in clinical practice rather than for experimental work, physiology, or anatomical purposes”. The IASP’s preamble is not clear about how the definition is to be employed in clinical practice. If Merskey and Wall are representative of the intended use, it is not by identifying a treatment target. If we accept Merskey and Wall’s claims above at face value, we may instead take the role to be, simply and as claimed, to capture common usage. We’ll return to the role of pain reports in the clinic in the concluding chapter. Setting this positive role aside, central for this chapter’s purposes is the explicit introduction about what the definition is not intended for: research. The definition was simply not intended to offer something to which scientific generalisation may usefully refer: it was explicitly not intended for scientific research.

164  Adopting Scientific Eliminativism Indeed, one reading of Anand and Craig’s criticism of the definition takes it to stem from their very dissatisfaction with its limited aim. Thus, in response to Merskey and Wall’s defences, they write (1996b, p. 210): Whereas common usage of the word ‘pain’ has to be learnt from early experiences and has remained unchanged for thousands of years, the scientific definition of this phenomenon must go beyond the semantic use of a word to the core of the experience. Setting concerns about the semantic methodology enshrined in this passage aside, Anand and Craig’s point is that the referent for ‘pain’ identified by the IASP is inadequate as a referent of ‘pain’ for scientific inquiry. A ‘scientific definition’ of pain has to go beyond the purely subjective report. As I hope has become clear from the discussion above, however, it seems to me that Anand and Craig err if they think Merskey and Wall here disagree with them. The IASP definition, as we might put it, was never intended as a “scientific definition”—it was explicitly offered under the proviso that it wasn’t for and shouldn’t constrain scientific inquiry. Whether or not the definition was intended to identify something usefully referenced in scientific generalisations, however, the more important question is whether it does so. Whatever the stated aims of the IASP task force, and however the definition is understood by advocates like Wall and Merskey, it should be admitted that scientists have often trotted out the IASP definition as if it were a ‘scientific definition. As if, that is, the definition identified something which is usefully referenced by the deployment of ‘pain’ and other pain terms in their offered generalisations. The definition, even if accepted, does no such thing. Consider the nature of the posited referent. It seems to me flatly incredible that it would be useful for any scientific generalisations to refer to a non-physical, non-biological, non-observable, purely subjective entity for which the subjective report is the only valid indicator. Consider if the only valid marker for any other purported kind of our biological and neural sciences was the subjective report. Imagine, for instance, if this were accepted for cancer, diabetes, or any other biological malady. It would, I submit, be unacceptably absurd. Imagine, going further, if it were proffered even as the definition of any other type of mental episode, e.g. vision or olfaction. You see whatever you say that you see, and what you see is—even in principle—poorly correlated with any neural activity, physical process, or behavioural pattern. Were we to accept such claims, it seems to me that we would be accepting the rejection of the very possibility of vision science. To accept the IASP definition, it seems to me, is to accept that pain—as posited by our everyday theory—does not pick out a referent which is useful for scientific explanation or prediction.

Adopting Scientific Eliminativism  165 Murat Aydede (2017) has recently defended the IASP definition using philosophical argument. He claims that what all pains have in common is their phenomenology—that is, what it is like for one, from the inside, to have the pain. He then further claims that phenomenology is only directly accessible through first-person reports—that is, the only way to get a grip on what it’s like for someone else is for them to tell you what it’s like for them from the inside. Consequently, he thinks it appropriate to accept that there is no valid biological, physical, or observable marker for pain. None of these will get to what it’s like for a person to be in pain. Aydede thinks that the IASP definition does a good job of capturing these features.16 Central for present purposes is that even were we to accept all of this, we should still accept scientific eliminativism for the reasons given in the previous section. Again, accepting the IASP definition and Aydede’s claims seems, if anything, to support scientific eliminativism. For consider: if pain is a phenomenological kind which is not well-correlated with any biological, neurological, or any other scientific kind, then shouldn’t we cease referencing it in scientific generalisations? If we accept the IASP definition of pain, then we do best to follow Wall, Merskey, and those who have advocated and defended the definition as one which characterises pain as referenced in everyday life, but which does not identify a treatment target or anything else usefully referenced for scientific research. Though not central for present purposes, given its influence, I want to further note that I think we should reject the IASP definition—even as an accurate characterisation of pain as posited in our everyday lives. In brief, this is because our everyday posit of pain is both more variable and less subjective than the referent identified by the IASP definition of ‘pain’. As discussed in Chapter 1, we accept a wide range of episodes as pains in everyday life. And though a paradigmatic pain will be unpleasant, we’ve now seen—as in reports of pain asymbolia and morphine pain— that not all pains are taken to be unpleasant by those who report them or those who accept their reports. Going further, though a paradigmatic pain will have a sensed location, in everyday life we often accept reports of emotional pains, as real pains, despite their lack of a particular sensed location: the pain of my grief may be utterly overwhelming. In everyday life, that is, we do not require of a pain that it be associated with tissue damage—even potential tissue damage. There is, as far as I can tell, also no particular emotion which we require all pains to have associated— though many of us may find the masochistic report of one who takes joy in their pains to be unusual, I submit that we do not find this report to be unintelligible. I also argued in Chapter 2 that we should reject the idea that pains are all and only those episodes with a distinctive qualitative character, such that there is a distinctive way they are like for one when conscious, i.e. I argued against the orthodoxy of simplicity. If Aydede is

166  Adopting Scientific Eliminativism right that the best interpretation of the IASP definition commits them to this orthodoxy, then we should reject the definition on those very grounds. So too and finally, in deeming pain to be a purely subjective phenomenon about which we are incorrigible and infallible, the IASP definition has arguably become unintelligible. Many in philosophy questioned whether such a report would be a meaningful report at all.17 If the only requisite condition for my being in pain is, strictly, my sincerely saying that I’m in pain, then it’s unclear what there is to my being in pain beyond my saying so. But surely, in our everyday lives, we think there is more to my being in pain than my merely saying so: when I tell you that I am in pain, I tell you something about what’s going on with me—something that I think I am accurately reporting by saying that I am in pain. We’ll consider pain as posited in our everyday lives in more detail in the next chapter. For now, I conclude that the IASP definition needn’t trouble the scientific eliminativist for pain or any pain type. According to the IASP definition, pain is a purely subjective psychological phenomenon which is poorly correlated with any physical process, neural activity, biological marker, or any observable phenomenon whatsoever. The definition was explicitly intended to capture common usage of the term ‘pain’. As seen in previous chapters and explored yet further in the following, however, our everyday theory of pain takes it to be both more variable and less subjective than the IASP definition claims. Most centrally for the purposes of the present chapter, the IASP definition, even if accepted, fails to identify anything which is usefully referenced in scientific generalisations. If anything, accepting the IASP definition may provide further reasons to accept scientific eliminativism for pain and pain types. 4.3.2 The Flourishing of Pain Science An important objection may have long been brewing. Pain science is flourishing. Substantial progress has been made—indeed, some of this progress has been canvassed in the preceding pages. Developments in pain science have increased our understanding of the brain, the nervous system, primary afferents, homeostasis, genetics, the functioning of the immune system, and much else besides. It might initially seem obvious that references to pain and pain types have been useful contributors to these developments. In short: doesn’t the utility of the investigations which refer to pain and pain types in their generalisations evidence the utility of those references? If so, then shouldn’t we recognise that pain and pain types are natural kinds, reject scientific eliminativism, and accept pluralism? This objection is important, but it is importantly misplaced. Pain science is flourishing and has made substantial progress. Inquiries into pain and pain types have been fruitful. Nonetheless, neither pain nor pain

Adopting Scientific Eliminativism  167 types are usefully referenced in the generalisation of any science. ­Instead, pain science has flourished despite references to pain as such or to pain types and not because of them. To clarify this response, set pain aside for a moment and consider two other posits from the history of science: luminiferous aether and the humours. Investigation into aether and the humours was useful and bore much fruit, but references to these in the generalisations of the relevant sciences were nonetheless not useful and were appropriately eliminated. Consider luminiferous aether; for ease, simply aether. The term ‘aether’ was originally canonically used to refer to a posited substance, made of numerous particles, which facilitated the travel of light. Many scientific inquiries into aether, so posited, were carried out—inquiries which bore fruit! Over time, however, as a result of the discoveries delivered through these investigations, scientists began to attribute increasingly complex and conflicting features to aether, and it became hard to see how anything could have all of those features. It was Einstein who seems to have eventually refuted its existence, that is, to have refuted the existence of anything which could have all of the features that the posited thing, aether, was by then supposedly discovered to have. It is worth noting that Einstein himself apparently pointed out that the scientific community could, if they wished, retain the term ‘aether’ and use it to refer to something similar, but different. The scientific community demurred, however, and the term simply ceased to be deployed in any scientific generalisations. Aether was determined not to exist, references to it were eliminated from scientific generalisations, and it was no longer the object of any scientific inquiries.18 Let us grant that the scientific community was here correct in ceasing to deploy the term ‘aether’ in any of its investigations and rejecting the aether posit. We are not thereby denying that previous inquiries or investigations targeted at aether were useful or fruitful. They were! Generalisations about aether and inquiries targeting aether may have been, for some time, the best that science could do. It was the useful investigations targeted at aether itself, however, that eventually showed that we should reject the posit. That is the nature of scientific progress. Physics, we learned, could do better. Briefly consider the humours. On into the twentieth century it was widely believed that there were four basic substances in the body dubbed the humours: black bile, yellow bile, phlegm, and blood.19 Health was explained by their balance, and their imbalance was theorised to result in various maladies. This theory, called humourism, is ancient and litters the history of medicine. It is now accepted that humourism is false: humours are not a useful posit, and the humours are no longer accepted as an appropriate object of scientific inquiry. As with Einstein’s suggestion for ‘aether’, notice that we could, if we wanted, have retained the term ‘humour’ and changed its referent. Most intelligibly, perhaps, to

168  Adopting Scientific Eliminativism something similar but distinct, such as blood. The scientific community has, however, again opted to drop the term altogether. Enough of humourism has been discredited that scientific eliminativism for the humours was adopted. Notice yet again that despite the appropriateness of adopting scientific eliminativism for the humours, there have been many investigations into the humours—investigations which were useful and fruitful! This should not be denied. Nor, on this basis, should scientific eliminativism for the humours be rejected. Generalisations about the humours and inquiries targeted at them may have been, for some time, the best that science could do. Useful investigations of the humours themselves, however, eventually showed that we should reject humourism and its posit of the humours. This is the nature of scientific progress. Biology, we learned, could do better. One moral of these short stories is that investigations into a posited kind may be more or less useful at different times. One thing which may happen is that investigations into the posited kind become increasingly useful over time. We have learned more and more about, e.g., bones, water, iron, trees, tigers, and so on. References to these kinds has, correspondingly, become increasingly useful for explaining and predicting a wider range of things with a greater degree of success. This is, perhaps, the way one may have expected scientific progress always to look. As the cases of humours and aether illuminate, however, investigations into a posited kind may instead become of decreasing utility over time. Scientific investigation into these kinds eventually revealed that we should cease to investigate them altogether. References to these kinds were revealed not to be useful for explanation and prediction; instead, as we investigated these kinds, we discovered other, more useful referents for explaining and predicting. We discovered that the relevant sciences could do better. Investigations into aether and the humours were useful and fruitful. In recognition of this utility, it may be tempting to say that references to these kinds in scientific generalisations were likewise useful. Doing so, however, conflates the utility of the investigations with the utility of the references. Given what these investigations have taught us about the world, we should not credit the utility of these investigations to references of these kinds; rather, credit belongs to the things that the investigations into these kinds allowed us to discover despite these references. Rather than say that references to these posited kinds were ever useful, it is better to say that investigations into these kinds were useful despite these references. We of course thought that referring to aether and the humours was useful, but we were wrong. Our very investigations into these posited kinds led us to that discovery. Recall that the liberal scientific utility criterion with which we are working stipulates that a kind is natural insofar as it is usefully referenced

Adopting Scientific Eliminativism  169 in scientific generalisations for explanation and prediction. We can now see that when an investigation is useful and fruitful, this may tempt us to conclude that the kinds posted in the investigation are natural. This will sometimes be the case—as we now take it to be, for instance, with bones and tigers. But it will sometimes not be the case—as we now take it to be for aether and the humours. We should stand behind our best theories at, but only at, a given time. We may simply be wrong, at any given time, about which kinds are natural. We may, that is, simply be wrong about whether references to a posited kind are useful for scientific explanation and prediction. As science progresses, our posits improve. Sometimes we uncover evermore reason to accept that a posited kind is natural, i.e. we discover evermore reason to accept that they are usefully referenced in scientific generalisations. Sometimes, however, inquiry will lead to evermore reason to think that the posited kind is not natural, i.e. they are not appropriate objects of scientific inquiry. And, indeed, since utility itself comes in degrees, this too may be something which inquiry may reveal, i.e. some kinds are more or less usefully referenced for explanation and prediction than others. These are all things we discover about our posits over time, as science progresses. Returning to pain: the utility of scientific inquiries into pain and pain types should not be denied. We should not simply conclude from this, however, that pain or any pain types are natural kinds. We should not, that is, simply conclude from the utility of scientific investigations targeted at pain that references to pain or pain types in scientific generalisations are useful for explanation and prediction. As with aether and the humours, it may be that investigations targeted at pain and pain types have been useful and fruitful despite these references. If the arguments in the previous section are correct, this is exactly what we should conclude. The utility of scientific investigations into pain and pain types is, by itself, perfectly consistent with the flourishing of pain science. In addition to the arguments already offered, notice that the history of pain science itself suggests that pain science has progressed despite, and not because of, references to pain and pain types. The recent history of pain science has witnessed progress from narrow, restrictive understandings of pain as a particular sensation, with dedicated receptors, pathways, and neural areas to an understanding of pain as involving multiple different components, variously weighted, for distinct individuals on distinct occasions. Freeing ourselves from overly restrictive theories has allowed the development of novel treatments interventions, which are appropriate in some cases and not in others. Continuing inquiry has revealed that different token pains vary dramatically in their dynamics, neural involvement, appropriate treatment interventions, causes, effects, and so on. Our understanding of the mechanisms implicated in some, but not other, pains has dramatically advanced. Our

170  Adopting Scientific Eliminativism generalisations about these mechanisms are increasingly reliable and successful. All of this constitutes progress. But it is difficult to see any of the progress in pain science as vindicating the utility of generalisations about pain or pain types. Instead, developments suggest the deconstruction of pain as such or pain types into the component mechanisms which may idiosyncratically converge in distinct cases. As with aether and the humours, I contend that it is the scientific inquiries into pain and pain types which have themselves revealed that they are not usefully referenced in scientific generalisations. Utility will increase if we eliminate references to pain and pain types from our scientific generalisations, so long as we retain references to those mechanisms we have discovered to be implicated in some token pains. Generalisations about pain and pain types, and inquiries targeted at these, may have been, for some time, the best that science could do. Useful investigations into pain itself, however, revealed the complex idiosyncrasy which undermines the utility of references to pain or pain types in scientific generalisations. Biology, anatomy, pharmacology, anaesthesiology, and the many other relevant sciences can all do better.

4.4 From Pain Science to Pain in Everyday Life and Medicine Pain science itself, I have been arguing, reveals that neither pain nor any type of pain is usefully referenced in scientific generalisations. Multiple mechanisms idiosyncratically converge to determine each token pain, such that generalisations about either pain as such or pain types are inevitably inadequate for explaining and predicting pain. References to pain and pain types should be eliminated, though references to those mechanisms discovered to be implicated in pain should be retained. We have been lumping token pains together into groupings and seeking to offer generalisations about them. We do better to break the lump apart, recognise token pains for the complex idiosyncratic phenomenon that they are, and seek scientific generalisations about those mechanisms which may, or may not, be implicated in any token pain experiences. The idiosyncratic mechanistic differences across token pains undermine the utility of scientific generalisations about pain types or pain as such. Pluralism for these should be rejected in favour of scientific eliminativism. Accepting scientific eliminativism for pain and pain types, however, raises a significant worry which takes us to the following chapter. In particular, we might worry that if we should eliminate references to pain and pain types from science, then it follows that we should eliminate references to them from everyday life. Quite unlike aether or the humours, pain is not a posit of one of our specialised theories, but is instead a posit of our everyday theory of ourselves. Has science shown that pains simply don’t exist? This worry might impress itself upon us most strongly if we

Adopting Scientific Eliminativism  171 are naturalists: isn’t science, as we might put it, our best guide to what exists? If it’s not useful to refer to pain for scientific inquiry, then must the naturalist conclude that it simply doesn’t exist at all? But this seems absurd. In the following chapter, I’ll argue that we sometimes usefully and successfully refer to pain in everyday life, despite the fact that we should eliminate references to pain from scientific inquiry. Pain is real, though it is really complex and idiosyncratic.

Notes

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www.iasppain.org/AM/Template.cfm?Section=Pain_Definitions&Template= /CM/HTMLDisplay.cfm&ContentID=1728#Pain

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Adopting Scientific Eliminativism  173 Bechtel, W. (1994). Levels of description and explanation in cognitive science. Minds and Machines, 4(1), 1–25. Blom, S. M., Pfister, J. P., Santello, M., Senn, W., & Nevian, T. (2014). Nerve injury-induced neuropathic pain causes disinhibition of the anterior cingulate cortex. Journal of Neuroscience, 34(17), 5754–5764. Chahl, L. A. (1996). Opioids-mechanisms of action. Australian Prescriber, 19(3), 63–65. Craver, C. F. (2007). Explaining the brain: Mechanisms and the mosaic unity of neuroscience. Oxford University Press. Dupre, J. (1993) The disorder of things: Metaphysical foundations of the disunity of science. Harvard University Press. Eccleston, C., & Crombez, G. (1999). Pain demands attention: A cognitive– affective model of the interruptive function of pain. Psychological bulletin, 125(3), 356. Ereshefsky, M., & Reydon, T. A. (2015). Scientific kinds. Philosophical Studies, 172(4), 969–986. Fodor, J. A. (1974). Special sciences (or: The disunity of science as a working hypothesis). Synthese, 28(2), 97–115. Hassenbusch, S. J., Stanton-Hicks, M., Covington, E. C., Walsh, J. G., & Guthrey, D. S. (1995). Long-term intraspinal infusions of opioids in the treatment of neuropathic pain. Journal of Pain and Symptom Management, 10(7), 527–543. Machery, E. (2009). Doing without concepts. Oxford University Press. Marr, D. (1982), Vision: A computational approach, San Francisco, Freeman & Co. Merskey, H. (1996). Response to editorial: New perspectives on the definition of pain. Pain, 67(1), 209. Nutton, V. (2013). Humoralism. In Companion encyclopedia of the history of medicine, edited by W. F. Bynum (pp. 307–317). Routledge. Rosenthal, D. (2010). How to think about mental qualities. Philosophical Issues, 20(1), 368–393. Sundstrom, R. R. (2002). Race as a human kind. Philosophy & Social Criticism, 28(1), 91–115. Wall, P. D. (1996). Response to editorial by Anand and Craig. Pain, 67(1), 209. Whittaker, E. (1989). A history of the theories of aether and electricity: Vol. I: The classical theories; Vol. II: The modern theories, 1900–1926 (Vol. 1). Courier Dover Publications. Wittgenstein, L., & Anscombe, G. E. M. (1953). Philosophical investigations. London, Basic Black. Woolf, C. J., Bennett, G. J., Doherty, M., Dubner, R., Kidd, B., Koltzenburg, M., & Torebjork, E. (1998). Towards a mechanism-based classification of pain? Pain, 77(3), 227–229. Woolf, C. J., & Mannion, R. J. (1999). Neuropathic pain: Aetiology, symptoms, mechanisms, and management. The lancet, 353(9168), 1959–1964. Woolf, C. J., & Max, M. B. (2001). Mechanism-based pain diagnosis issues for analgesic drug development. Anesthesiology: The Journal of the American Society of Anesthesiologists, 95(1), 241–249.

5

Rejecting Traditional Eliminativism Why Pain Is Still Real

5.1 Introduction As I’ve repeatedly noted, pain is a posit of our everyday theory. We didn’t discover it in the lab or posit its existence for some specialised purpose. In the course of our everyday lives, we report pains that we take ourselves to have, and we attribute them to others. We teach our children to identify and report pains on those occasions when they—apparently to us—express them, and correct them when they report pains on occasions when they—apparently to us—are not undergoing them. It is part of our accepted, everyday wisdom that being in pain may cause the pained to do things, e.g. curse, cry, or seek help. It is part of our accepted, everyday wisdom that some things can cause pain, e.g. getting hit in the head, cutting a finger, or labour. Pain plays a well-accepted role in our everyday way of thinking about ourselves, and we often and effortlessly appeal to it for explaining and predicting each other’s behaviour. As we’ve also repeatedly seen, this everyday posit of pain is promiscuous: a wide range of diverse episodes are accepted, in everyday life, to be pains. A wide range of diverse episodes, that is, are taken to play the well-accepted role sketched above, previously described, and known to us all from everyday life. We saw in Chapter 1 that one among many consequences of this is that our everyday theory of pain does not settle all the questions about pain’s nature which we may ask. We saw in Chapter 2 that in grappling with such questions, philosophical theories of pain have taken pains to be all and only those mental episodes with a certain quality—dubbed, the pain quality—and attempt to give an account of that quality. I’ve argued that this orthodox specification of the nature of pain is too simple. We should reject the orthodoxy of simplicity and, instead, follow everyday theory in accepting that pain is itself complex. Enriched through discoveries from pain science, we should accept that pain itself has multiple, dissociating components which converge idiosyncratically to determine each token pain. The complex idiosyncrasies of token pains, however, constitute difficulties for specialised inquiries into pain’s nature including not only philosophy, but the sciences. As we saw in Chapter 3, the complex

Rejecting Traditional Eliminativism  175 idiosyncrasy of pain, itself discovered by pain science, nevertheless undermines the mechanistic explanations of pain or pain types at which scientific inquiries into pain have often aimed. As we saw in Chapter 4, this same complex idiosyncrasy also undermines the utility of generalisations about pain or pain types for the explanations and predictions at which the sciences aim. Neither pain nor any type of pain, as we might more technically and succinctly put it, is a natural kind. For pain science, we do best to eliminate references to pain as such or to pain types, and instead seek to offer explanatory and predictive generalisations about the mechanisms implicated in pain. Indeed, investigations into these contributory mechanisms are flourishing. The difficulties for specialised philosophical or scientific theories of pain, however, may lead us to doubt our everyday theory’s very posit of it. Perhaps pains are not only complex and idiosyncratic; perhaps there is something incoherent or internally problematic about our everyday notion of pain. Recognising that there is no biological marker or mechanistic explanation of the pains that we take ourselves to have may seem a particularly compelling reason to think that there just aren’t any. We thought there were pains, but we were wrong. Scientific inquiry has instead unearthed multiple, dissociating mechanisms, differently associated with pain on different occasions, but no one or combination of which is reliably correlated with pains as posited in our everyday lives. By deploying the scientific method to limn the nature of pain, we identified only other things instead. Doesn’t that show that pains simply don’t exist? In short, if science doesn’t usefully offer generalisations about pains, then perhaps we shouldn’t accept their existence in our everyday lives either. This chapter addresses these doubts. To begin addressing these concerns, it is important to distinguish between the scientific eliminativism, on which the previous chapter focussed, and traditional eliminativism. Scientific eliminativist arguments, as we’ve seen, conclude that a kind is not natural and, accordingly, that we should eliminate references to the kind from scientific discourse. Traditional eliminativist arguments go further. These conclude that we should eliminate reference to something even from our everyday discourse on the grounds that it doesn’t exist. If something doesn’t exist, then we can never successfully refer to it—not in science, not in medicine, not in daily life, and not ever. To be a scientific eliminativist about pain or pain types is to hold that references to them are not useful for scientific inquiry. To be a traditional eliminativist about pain, however, is to hold that there are no pains—so references to them, as if there are, should be eliminated. And, of course, if there are no pains, then there are no types of pain either. Scientific eliminativism may itself be thought to be a good reason for traditional eliminativism. Remember that in the last chapter we briefly considered the idea that one reason, though not the only reason, to be

176  Rejecting Traditional Eliminativism a scientific eliminativist about a kind is if none of its members exist. If there are no pains, then it’s not useful to have a science of pain. But as seen above, the reverse line of reasoning is also tempting: if the posited kind is not usefully referenced in scientific generalisations, then perhaps that’s a good reason to think that the posited kind has no existing members. Perhaps the supposed members of posited kinds which aren’t natural simply don’t exist. The idea is that if we can’t have a useful science of something, then that something doesn’t exist. For pain in particular: if we are scientific eliminativists about pain, perhaps we should also be traditional eliminativists about pain. Some philosophers have responded to the developments in pain science by adopting traditional eliminativism for pain. Daniel Dennett (1978), in the wake of gate-control theory, offers the classic version of the view, and Valerie Hardcastle (1999) offered a more recent version. Both Dennett and Hardcastle deploy evidence from pain science to argue that our everyday posit of pain is problematic beyond revision. On this view: the pains that we take ourselves to successfully reference in our everyday lives simply do not exist, and we should, accordingly, eliminate such references. Traditional eliminativism for pain might seem incredible. As noted at the end of the previous chapter, pain is a posit of our everyday theory and the denial that it exists—on scientific or any other grounds—might seem flatly absurd. Could we really ever discover that pains don’t exist? Is this even an idea that we should be taking seriously? However incredible it may initially seem, traditional eliminativism for pain is worth taking seriously. Our everyday theories of ourselves and our world are fallible. We have, sometimes, gotten it wrong about what exists. Indeed, just briefly consider: why think that we couldn’t get it wrong?1 Witches are often offered as a classic example. 2 It was, in some times and places, taken to be an accepted part of everyday wisdom that there were certain women who had made a pact with the devil and sent out their spirits to make mischief. Many appealed to witches for everyday explanation and prediction. We now know that they were wrong. Particular women were considered to be members of the posited kind witch, but we now know there are no witches. The kind witch has no members. There were always, instead, only particular women—who, in many cases, were in some way socially unacceptable and died for it.3 Our posit of witches is of course only a single example, but it is sufficient to see that our everyday theory is fallible. Having rightly accepted the fallibility of our everyday theory, we might think the best way to test its posits is to submit them to scientific inquiry. Science, we might think, is the final arbiter of what exists. As above, that is, we might think that if a kind is not natural, then its members simply don’t exist: anything not usefully referenced for scientific explanation and prediction must simply not exist at all.

Rejecting Traditional Eliminativism  177 On this sensible line of thought, if the argument in the previous chapters is correct, then we should conclude that there are no pains, however incredible or absurd that may initially seem. Perhaps it is a surprising scientific discovery that pains, like witches, don’t exist. There are women deemed unacceptable by their societies, but there are no witches. So too, there may be many things in the neighbourhood—thermal sensations, unpleasant feelings, bodily damage, the motivation to protect our body, anxiety, and so on—but there are no pains. Especially in the light of scientific eliminativism for pain, traditional eliminativism for pain should be taken seriously. In this chapter, I nonetheless argue against traditional eliminativism for pain. I argue that pains, though complex, idiosyncratic, and non-natural, are nonetheless real. In the following two sections, I argue in turn against Dennett and Hardcastle’s traditional eliminativism. I show that, at best, these arguments support scientific eliminativism. In Section 5.4, I turn directly to whether scientific eliminativism entails traditional eliminativism. Must we either reject scientific eliminativism for pain or accept that pains don’t exist at all? Fortunately not. Instead, I submit that even as the question of scientific eliminativism rightly turns on the question of scientific utility, so the question of traditional eliminativism righty turns on the question of everyday utility. Science is not the only explanatory and predictive purpose for which we refer. Instead, some things that should be eliminated from scientific discourse are nonetheless usefully referenced for explanation and prediction in everyday life—and any references earning their explanatory and predictive keep should be accepted as successful references. We should accept that pains exist if it is useful to reference them for explanation and prediction in daily life. And, it is. Pain science itself has revealed that each token pain, as posited by our everyday theory, is explained by the idiosyncratic convergence of the activity of multiple mechanisms. While this discovered complex idiosyncrasy of pain undermines useful scientific generalisations about pain and pain types, those complex idiosyncratic experiences are nonetheless usefully and successfully referenced in everyday life. Pains are complex and idiosyncratic, but they are real for all that.4

5.2 Dennett’s Pain Eliminativism Dennett’s traditional eliminativism for pain is characteristically subtle; he sometimes sounds as if he thinks that pains exist after all. Nonetheless, it seems clear to me that the best interpretation of him is as proffering traditional eliminativism for pain. Two arguments for traditional eliminativism for pain can be extracted from Dennett’s impressive work. The first relies on his distinction between personal and sub-personal levels of explanation. He argues that pain is a personal, non-mechanistic phenomenon that is not appropriately

178  Rejecting Traditional Eliminativism identified with any of the sub-personal, mechanical events or processes in the brain or body. Since it is to the mechanistic, scientific categories that Dennett maintains we are to look to determine what exists, he concludes that pains do not exist. His second argument focusses on a specific reason that he thinks the non-mechanical, person-level phenomenon of pain will not submit to identification with any mechanical, sub-personal processes—namely, that we cannot have a true theory of pain, even at the personal level. Our ordinary notion of pain is argued to be riddled with deeply entrenched contradictions. Since no true theory is contradictory, Dennett concludes that there is no true theory of pain. We’ll consider each of these arguments in turn. To consider Dennett’s arguments, we need to get a working grip on the distinction between the personal and the sub-personal. This distinction has been put to different uses by different philosophers, and it is not easy to give an agreed characterisation of it. Indeed, interpretation of even Dennett’s own use of the distinction is controversial.5 For our purposes, however, we can be rather broad. We’ll take personal-level explanations to be explanations of behaviour which posit states, processes, or functions of the whole person, and sub-personal explanations to be explanations of behaviour which posit states, processes, or functions of some component of the person. Similarly, we’ll take a personal-level phenomenon to be one that is posited of the whole person to explain their behaviour and a sub-personal level phenomenon to be one that is posited of a component of the person to explain their behaviour. Love, for example, is a personal-level posit of our everyday theory: persons, but no components of persons, love, and love receives appeal to explain and predict the behaviour of persons, but not any of their components. When Dennett first introduces the distinction between personal and sub-personal levels of explanation (1969), pain is offered as a paradigmatic example of a personal-level phenomenon. Persons feel pain; pain is not experienced by a component of the person, nor is it rightly identified with any of the workings of a component, or indeed multiple components, occurring within the person. Crucially, these facts together are presumed to block successful inquiry into the mechanics of pain, since mechanical questions are raised and answered at the sub-personal level. He writes (1986, p. 63): An analysis of our ordinary way of speaking about pains shows that no events or processes could be discovered in the brain that would exhibit the characteristics of the putative ‘mental phenomena’ of pain, because talk of pains is essentially non-mechanical, and the events and processes of the brain are essentially mechanical. I’ve argued in Chapter 3 that pains do not submit to mechanistic explanation, but what are Dennett’s reasons for thinking so?

Rejecting Traditional Eliminativism  179 According to Dennett, mechanistic explanation for pain is blocked because our everyday theory is committed to pains being a ‘brute and unanalysable’ experience. Both how we identify our mental episodes as pains and what it is to be a pain are—according to our everyday theory and according to Dennett—nothing that can be analysed or broken down into functional, mechanical processes. According to Dennett, this claim is so central to our everyday theory of pain that if we give it up, then we won’t be talking about pain anymore. The brute, unanalysable— and so non-mechanical—nature of pain is an essential part of our everyday theory. So, he writes (p. 65): … when we abandon the personal level in a very real sense we abandon the subject matter of pains as well. … our alternative [sub-personal, mechanistic] analysis cannot be an analysis of pain at all, but rather of something else—the motions of human bodies or the organization of the nervous system.…Abandoning the personal level of explanation is just that: abandoning the pains and not bringing them along to identify with some physical event. … The ordinary concept of pain, therefore, does not succumb to mechanical explanation. How does Dennett then move from the idea that pains cannot be mechanistically explained to the idea that pains do not exist? According to Dennett, we shouldn’t look to our everyday theory—which includes the posits of personal level phenomenon, like love and pain—to determine what exists. Rather, we should look to scientific theory—and its posits of sub-personal level phenomenon. Any personal-level phenomenon posited by our everyday theory which we cannot identify with the sub-personal level phenomenon posited by science does not exist. And all sub-personal level phenomenon, according to Dennett, are mechanistically explicable. That those mental posits which exist will eventually be mechanistically explained through scientific inquiry seems to be taken by Dennett as simply obvious. He writes (p. 41), for instance: This much ought to be uncontroversial; though psychologists may ignore the details of realizations while elaborating and even testing their models, the model making is ultimately bound by the restriction that any function proposed in a model must be physiologically or mechanically realizable one way or another. Either pains, as posited by our everyday theory, are identical to something in our scientific theory or they are not. If they are, then they would be mechanistically explicable. But, according to our everyday theory, they are essentially not mechanistically explicable. So, identity is out and they must not be identical to anything in our scientific theory. And in

180  Rejecting Traditional Eliminativism that case, they don’t exist at all. He makes this clear in concluding the discussion by writing (p. 66): The only way to foster the proper separation between the two levels of explanation, to prevent the contamination of the physical story with unanalysable qualities or ‘emergent phenomena’, is to put the fusion barrier between them. Given this interpretation it is in one sense true that there is no relation between pains and neural impulses, because there are no pains; ‘pain’ does not refer. There is no way around this. If there is to be any relation between pains and neural impulses, they will have to be related by either identity or non-identity, and if we want to rule out both these relations we shall have to decide that one of the terms is non-referential. The last piece of the puzzle to explain is the “fusion barrier” to which he here eludes. This barrier is central to the homuncular functionalism about the mind that Dennett advocates. Homuncular functionalism, roughly, is the idea that we start our theorising about the mind using our everyday mental terms, and then we break down the posits to which those terms refer into increasingly compartmentalised functional components— as guided by scientific inquiry. As scientific inquiry into these posits of our everyday theory progresses, we identify components that are more and more ‘stupid’, i.e. less mental, personal, and intentional. Scientific inquiry is thus taken to facilitate the ‘fusion’ of the mental, personal-level posits of our everyday theory into those at the mechanistic, sub-personal level. Our everyday theory uses terms to refer to posits with which our scientific investigations of the mind begin. (Indeed, one might wonder, where else inquiry into the mind could begin.) Submitting these to investigation will, when the posits exist, yield mechanistic explanations. Some of the posits of our everyday theory are unproblematic: those that can be ‘fused’. Dennett’s traditional eliminativism for pain, then, is not based solely on the fact that it is a personal-level phenomenon. Some personal-level phenomena and the terms that refer to them are acceptably fused into the mechanical, functional explanations provided by scientific inquiry. Beliefs, for instance, are fine; these can be fused without our changing the subject. The problem with pain is that it can never be fused into a mechanical explanation. In the case of pain, when we try to fuse, we inevitably change the subject. There is no sub-personal, mechanistic explanation for pain. Since we should look to scientific posits to determine what exists, and all of these posits do admit of a mechanistic explanation, then we are forced to concede that pains simply don’t exist. Dennett’s first argument for traditional eliminativism for pain, then, proceeds as follows: we started with pain as posited by our everyday theory,

Rejecting Traditional Eliminativism  181 found that it is not mechanistically explicable and so unsuitable for science, and reject the existence of pain because of its scientific unsuitability.6 I agree with Dennett that pains are not mechanistically explicable (as argued in Chapter 3) and that they are not suitable posits for scientific inquiry (as argued in Chapter 4). If the move from scientific eliminativism to traditional eliminativism is a good one, it’s one that could as easily be made on the basis of the arguments for scientific eliminativism that I myself have provided. We’ll turn in Section 5.4 to whether the move is in fact a good one, i.e. whether we should conclude that a posit of our everyday theory doesn’t exist on the grounds that it is not usefully referenced for scientific explanation and prediction. Consider now, however, Dennett’s offered reasons for scientific eliminativism. Dennett thinks that pain, as posited by our everyday theory, is an unsuitable posit for science because he thinks that pains are not mechanistically explicable, and that scientific inquiry (at least of the mind) delivers mechanistic explanations.7 The presented reasons for holding that pain is not mechanistically explicable, however, all concern his construal of our everyday theory. In particular, Dennett holds that our everyday theory of pain is committed to the claim that pains are essentially unanalysable mental qualities that are brutely discriminated. But why should we think that? Dennett does not offer any reasons. We should, at the very least, be suspicious of these claims, since ‘essentiality’, ‘mental quality’, ‘unanalysable’, and ‘brutely discriminated’ all reek of the vocabulary of the specialised theorist and not of our everyday theory. Dennett’s first argument rests on this claim about our everyday concept, but it receives no support. Dennett’s second argument for traditional eliminativism for pain rests even more directly, and obviously, on his construal of our everyday theory. In his classic (1978), he argues not only that pains as posited by our everyday theory will not admit of mechanistic explanation, but that our everyday theory of pain is contradictory beyond revision. In this argument, the problem with our everyday theory’s posit of pain is prior to anything unearthed by scientific inquiry. According to our everyday theory, pains have contradictory features. But nothing has contradictory features, so pains—as posited by our everyday theory—don’t exist. I think Dennett is right that if our everyday theory of pain were contradictory beyond revision, then we should accept traditional eliminativism for pain. I deny, however, that the everyday concept of pain is contradictory beyond revision in the ways that Dennett alleges. Leaning heavily on the best science of the time, Dennett arrives at a complex model of pain involving the convergent activity of multiple mechanisms. Each of these mechanisms may be active independently of the others. Whenever this happens—and it frequently does—the model cannot be used to determine whether the resultant episode is pain.

182  Rejecting Traditional Eliminativism The  mechanistic model is thus inadequate for the legion dissociative cases. As further detailed in the previous chapters: so far, it seems to me, so good. An adequate theory of pain, according to Dennett, should nonetheless determine which combination of activations results in pain and which does not; it should allow us to say of each token episode whether it is pain or not. We may not expect this of the pain scientist or the clinician, but Dennett thinks that we expect it of the philosopher. To carry out their distinctive task and offer rulings on the dissociative cases, Dennett thinks the philosopher must determine what is essential to pain—a tricky business given all of the empirically discovered dissociations.8 Enter the rub. To determine what is essential to pain, Dennett claims that the philosopher must consult well-entrenched everyday intuitions as evidenced by everyday usage of the term ‘pain’. The allegedly fatal problem is that our ordinary, everyday intuitions about pain comprise an inconsistent set. Dennett identifies three contradictions in our everyday notion, and while he thinks the first two can be revised to salvage the everyday posit of pain, the third is irresolvable. In particular, our everyday notion of pain, according to Dennett, is unavoidably embroiled in the following contradiction: A B

Pains are essentially items of immediate experience or consciousness; the subject’s access to pain is privileged or infallible or incorrigible. Pains are essentially abhorrent or awful.

The contradiction between these may not initially be apparent. The problem rests in the rulings these intuitions yield in some dissociative cases. Dennett points to a range of dissociative cases, including those involving morphine, lobotomy, and pain asymbolia, that he thinks are best interpreted as evidencing a person both believing that they are in pain and experiencing something that is not awful. Dennett notes that not only do everyday people report these pains as not being awful, but other everyday people accept their reports. As we have already seen ourselves in early chapters, there are indeed many such dissociative cases. As nothing in the mechanical models will yield a principled ruling in the dissociative cases, the philosopher must consult our everyday theory, and the problem is that our everyday theory gives contradictory rulings. From A, if I believe that I am in pain, then I must be. From B, however, every pain is awful. A pain sincerely reported and believed to be non-awful is thus both a pain (by A) and not a pain (by B). According to Dennett, A and B are essential intuitions of our everyday theory of pain, such that we can’t reject or revise them. But as they contradict, Dennett holds that (p. 447) “[e]fforts to capture both of these ‘essential’ features in a theory of pain are bound to fail….”.

Rejecting Traditional Eliminativism  183 So, what should we do? Dennett advocates giving up not only these contradictory intuitions, but all of our everyday intuitions about what is essential to pain. He writes (448): I recommend giving up incorrigibility with regard to pain altogether, in fact giving up all ‘essential’ features of pain, and letting pain states be whatever ‘natural kind’ states the brain scientists find (if they ever do find any) that normally produce all the normal effects. Read in isolation, this passage suggests that Dennett is open to the possibility that pain scientists will eventually arrive at a true theory of pain, but this would be a poor reading in the context of the broader text and his other eliminativist argument above described. Instead, according to Dennett, any true theory will not be the true theory of pain, as posited by our everyday theory—though it may be a theory of something else that the folk will later begin to use the word ‘pain’ to reference. When we give up the (contradictory) essentiality claims about pain in favour of claims about the mechanisms being discovered by the scientists, we give up the everyday notion of pain. And, indeed, this is what Dennett thinks we should do. The idea is that we should reject the existence of pain as posited by our everyday theory—though we should also remain open to the idea that the word ‘pain’ might later be used, in science, to usefully reference something else. We should, that is, accept traditional eliminativism for pain. It seems to me that we should again question Dennett’s construal of our everyday theory. Why should we follow Dennett in accepting that A and B are essential to our everyday theory of pain? In particular, why accept that our everyday theory is essentially committed to pains being awful when, as Dennett himself discusses, there are dissociative cases of non-awful pains that everyday people report and countenance as pain? Everyday people, using our everyday theory, are apparently perfectly happy to accept that pains are typically or usually awful, but not necessarily so. Even if one—wrongly I think—maintained that everyday people are committed to pain having some essence or other, the very cases that Dennett points to for establishing the purported contradiction undermine the claim that our everyday theory saddles us with the essences he identifies. The very fact that everyday people accept reports of non-awful pains shows that Dennett’s attribution of essential awfulness is illegitimate. If the folk are not committed to the claim that pains are essentially awful, then dissociative cases do not support traditional eliminativism.9,10 I think we should reject both of Dennett’s arguments for traditional eliminativism for pain because both rely on illegitimate and unsupported claims about our everyday theory of pain. Nonetheless, as argued in the preceding chapters, I think Dennett is right that pain, as posited by our

184  Rejecting Traditional Eliminativism everyday theory, is not mechanistically explicable or usefully referenced for science. And Dennett, as noted above, holds that scientific eliminativism entails traditional eliminativism: he thinks that if scientific eliminativism is true, then traditional eliminativism must also be true. We’ll turn to this idea in Section 5.4. First, however, we’ll consider Hardcastle’s (1999) more recent eliminativism. I argue that here, too, everyday theory is illegitimately saddled with overly simplistic claims about pain and inappropriately blamed for the inadequacies of specialised pain metrics and diagnostics. Once everyday theory is freed from these burdens, the only remaining reason to accept traditional eliminativism is again scientific eliminativism. And, as I’ll argue directly in Section 5.4, that is not a sufficient reason.

5.3 Hardcastle’s Pain Eliminativism In The Myth of Pain, Hardcastle (1999) presents arguments both for a positive account of pain’s nature, intended for scientific discourse, and for traditional eliminativism for everyday discourse. According to Hardcastle, though pain can be appropriately salvaged for scientific inquiry, our everyday notion of pain must be rejected. Her position as stated appears to be a traditional eliminativism for pain, but without scientific eliminativism. As Tim Bayne (2000) points out, however, it is hard to see how Hardcastle’s traditional eliminativism is consistent with the positive proposal about pain that she offers for scientific inquiry. Hardcastle apparently claims that pain doesn’t exist, such that ‘pain’ never successfully refers. If so, however, then why does she continue to frequently use the term ‘pain’, and what is its referent when she does? If there are no pains, then what is her positive proposal a positive proposal of? By offering a proposal of pain’s nature, Hardcastle appears to be rejecting her own traditional eliminativist proposal. I take it that Hardcastle’s reply should be that her proposed referent of ‘pain’ for scientific inquiry is different than the referent of ‘pain’ as deployed when we are using our everyday theory. Since we used the term ‘pain’ in the process of identifying the complex, multidimensional experiences that Hardcastle thinks that we should accept do exist and which pain science should investigate, then we can go on using the term ‘pain’ to refer to these experiences. This is my best attempt to reconcile Hardcastle’s traditional eliminativism with her claim that pain is nonetheless usefully investigated by scientific inquiry (i.e. her rejection of scientific eliminativism), but I do not think it works. If the everyday concept of pain doesn’t pick out anything that actually exists, then the scientific research that she appeals to for establishing her positive proposal must not be about whatever everyday people (think they) are referencing with ‘pain’. But, notice then, though we might

Rejecting Traditional Eliminativism  185 retain the word ‘pain’ and use it to refer to something which does exist, we have changed the subject. In the aftermath of our scientific inquiry, the term ‘pain’ is no longer used to refer to the same thing. It would be like retaining the word ‘witch’ to refer to any women the speaker doesn’t like; we may choose to do so, but if we do, we are no longer referring to witches—as we indeed couldn’t, since there aren’t any. The moral is that one cannot consistently maintain that there are no pains, while still maintaining that pain has been discovered to be anything—even if the word ‘pain’ might be retained and be used to reference something else. Accordingly, Hardcastle must, I think, either give up her traditional eliminativism for pain or embrace scientific eliminativism for pain. She might, that is, claim that our everyday notion of pain has been discovered to successfully pick out something that science usefully investigates (consistent with her positive proposal for science), or she might claim that our everyday notion of pain does not pick out anything (in which case we should take her positive proposal for science as a model of something other than pain), but she cannot claim both consistently. If Hardcastle takes the first option, then she is no longer an eliminativist of any sort. For present purposes then, let us imagine that Hardcastle takes the second option and attempts to resolve the inconsistency by dropping the claim that her positive proposal is a positive proposal for pain. On this way of understanding her position, Hardcastle’s more recent pain eliminativist view is ultimately the same as Dennett’s classic version: we thought there were pains, made scientific inquiries, and to our great surprise discovered that there were none. When we went looking for pain, we found other mechanisms and processes instead, e.g., nociception, motivational signalling, and so on. Scientific inquiry thus revealed that while many associated mechanisms and processes exist (some of which we may choose to call ‘pain’), pains do not. On this reading, Hardcastle advocates both traditional and scientific eliminativism. In this section, I set my doubts about her positive proposal aside11 and argue that her arguments for traditional eliminativism anyway fail. One reason that Hardcastle offers for traditional eliminativism is that our everyday language for talking about pain is inadequate. She writes (pp. 151–153): The language we have for expressing our propositions concerning pain sensations is very crude.…We simply cannot express in a clear and unambiguous fashion how pain, in all its complexity, feels. … We simply do not have the language to express all the dimensions of our pain experiences. The descriptors are either metaphorical or nonexistent. Our folk [everyday] theory of pain needs to be replaced by something commensurate with the phenomenology [what our pains are like for us, at least when they are conscious].

186  Rejecting Traditional Eliminativism This reason for elimination is puzzling: how does the paucity of our language to describe our pains, even if granted, support that there aren’t any pains? Is it supposed that the word ‘pain’ somehow gets in the way of our ability to report our pains? This would, at least, be very surprising. If Hardcastle is right in this passage, then we apparently need more words to express our pains, not fewer. In short, even if our ability to express our pains is as impoverished as Hardcastle here contends, it is unclear how eliminativism would help. Going further: the concern that we are unable to adequately express or report our pains only seems to be appropriate if they exist. Consider next, however, as again noted by Bayne (2000) that Hardcastle is not always consistent in the way that she characterises our everyday notion. She sometimes appears to claim that we identify pain as a simple sensation, but at other times as complex perceptions. Many of her arguments for eliminativism, however, rely on characterising pain as a simple sensation that is necessarily conscious and necessarily awful. Thus, she writes (p. 154): …if what we refer to as pain turns out to be neither a conscious experience nor a perceptual simple, then what we are trying to point to in the world with the word does not exist, for these are the two defining features of our folk [everyday] notion of pain. Or again (p. 159): Though other aspects of our folk [everyday] psychology may not be wrong, our folk [everyday] theory of pain is woefully inadequate. We might play at revising this theory, but any change that remains faithful to what we know about pain processing is going to entail that pain no longer refers to a simple conscious percept. This sort of change crosses the line from mere revision to outright replacement. To support her overall view, then, I think she should resolve the contradiction by denying that she thinks we take pains to be complex perceptions in our everyday lives. Instead, our everyday posit of pain— according to this reading of Hardcastle—is of a simple, conscious, qualitative episode. Indeed, as per the two quotes above, this seems to be her more considered view of our everyday theory of pain. When her position is clarified in this way, however, we can see that the first problem with Hardcastle’s traditional eliminativism is the same as that which undermined Dennett’s arguments above: there seems no good reason, and none is provided by Hardcastle, to think that the resultant, problematic everyday notion of pain is the everyday notion. In particular, there seems no good reason to think that the folk are committed to the weighty necessity claims that she identifies. Why think that

Rejecting Traditional Eliminativism  187 our everyday theory is committed to the idea that pains are necessarily conscious, necessarily awful, or necessarily have a distinctive qualitative character? Notice again, as discussed in Chapter 1 and throughout: we accept a wide range of diverse episodes as pains in our everyday life. It is philosophers advocating the orthodoxy of simplicity, as discussed in Chapter 2, who come closest to accepting the simplistic characterisation of pain that Hardcastle takes to conflict with our best science. Hardcastle herself discusses dissociative cases which, note yet again, are all nonetheless accepted in our everyday life as pains. While philosophers may have offered overly simplistic theories of pain, there seems little reason to accept that our everyday theory is committed, much less essentially committed, to any such simplistic theory. While I think Hardcastle is right that a “…a good theory of pain” will not take pains to be simple, conscious percepts, no reason is provided for thinking that our everyday notion of pain does so. Our everyday theory of pain is not as narrow and simplistic as philosophers have made out.12 For reasons also given in previous chapters, however, I want to grant Hardcastle—like Dennett before her—that our everyday notion of pain does not well correspond to any of the mechanistic processes identified through scientific inquiry and that it is not usefully employed for scientific inquiry. While I again disagree about what our everyday theory of pain picks out, I agree that it isn’t something usefully referenced in science. How does Hardcastle reason to traditional eliminativism from scientific eliminativism? How does she reason from the idea that pain isn’t appropriately referenced in scientific inquiry to the idea that there are no pains? Hardcastle seems to think that if something is not appealed to in (presumably, any) scientific laws,13 then it does not exist. Science, again as in Dennett, is taken to be the ultimate authority concerning what does and does not exist. Decidedly unlike Dennett, however, Hardcastle further claims that it may be acceptable to refer to some things which do not exist in our everyday lives. She writes (p. 56): So far as I can tell, [one of the terms used in our everyday theory] not being a scientific term will have little impact on our common sense explanations of one another. ‘Folk’ [everyday] psychology, like other folk ‘sciences,’ need not be concerned with facts of the matter. It could function as well (or as poorly) as it ever did, regardless of whether intentional states really exist. The overall idea embodied in these and other passages seems to be that whether something exists depends on whether it is referenced in science’s laws, but that existence is irrelevant to the status of the posits of our

188  Rejecting Traditional Eliminativism everyday theory. Our everyday theory, Hardcastle seems to think, might be perfectly fine even if it refers to things that don’t exist. For everyday life, she seems to think, we don’t have to be concerned with ‘facts of the matter’. I confess to finding this a strange approach to our everyday theory and its role in our everyday lives. What could it mean to say that we successfully refer to something—successfully pick something out, attribute features to it, appeal to it for explaining and predicting each other’s behaviour, and so on—even though it doesn’t exist? How can we make sense of our everyday ways of understanding ourselves and each other as being unconcerned with facts about the way things actually are? It seems to me that if something doesn’t exist, then we shouldn’t continue to refer to it in everyday life for explanation and prediction—indeed, if something doesn’t exist, then we can’t successfully refer to it at all. Most relevant for present purposes, however, is that if Hardcastle’s way of thinking about our everyday theory is correct, then scientific eliminativism doesn’t entail traditional eliminativism. On this way of thinking, even if the posits of our everyday theory don’t pick out anything useful for scientific inquiry or which is appealed to in any scientific laws, the posits may still be perfectly fine. As I argue in the following section, I agree with Hardcastle that we should not reject our everyday posits on the grounds that they aren’t useful for scientific inquiry. As Hardcastle puts it (p. 156): We might not have a mental science or laws about pain, but our folk psychology [everyday theory] could still be used as it is now, in our everyday explanations of behaviour. It works well enough, in our specific cultural contexts, to get the job done. Hence, there is no need for elimination or replacement. On Hardcastle’s view then, unlike Dennett’s, there is room for the position that our everyday theory of pain is adequate for everyday life, even though pain is not usefully referenced in any scientific inquiry. Hardcastle seems to accept that some posits may be usefully referenced for everyday life despite failing to be usefully referenced for any scientific inquiry.14 So why doesn’t Hardcastle accept scientific eliminativism without traditional eliminativism for pain? As this is the very position advocated in this book, it is worth offering her direct response to it at some length. To the charge that the adequacy of our everyday theory of pain is left untouched by its lack of utility for scientific inquiry, she writes (p. 157): There is something undoubtedly right about this charge … [but there is] not enough to show that our folk ways of understanding pain are adequate. … for at least two reasons. First, people with pain

Rejecting Traditional Eliminativism  189 experiences that do not fit under our folk theories are assumed to have some psychiatric problem. Chronic pain without a diagnosed physical cause is deemed a mental disorder. Non-painful self-injuries are considered a mark of Borderline Personality Disorder. Second, the fact that different chemicals affect the qualitative experience of pain differently cannot be expressed using our folk measure of pain intensity, namely, how much it hurts. This has had serious consequences for patients trying to relieve their pain or suffering with drugs. I claim that there is a fundamental inadequacy to our folk theories. The burden is now on the folk psychologist to demonstrate how—despite appearances—our folk theories of pain are actually successful. The response to the objection that we ought to eliminate ‘pain’ from scientific theorising but not from everyday life, then, is that our folk understanding of pain is inadequate for (at least) two reasons: improper diagnosis and the inadequacy of intensity metrics to capture the complexity of pain as needed for treatment purposes. Hardcastle thinks pointing out these inadequacies is enough to shift the burden on to the defender of our everyday pain posit. This response is itself inadequate, however, because both of these offered reasons confuse our everyday theory and the everyday purposes to which it is put with the specialised purposes of the scientist and the specialised products of the clinician. In short, Hardcastle blames the purported inadequacies of the everyday notion of pain for the inadequacies of diagnosis and treatment, but this is inappropriate. Why blame our everyday notion for inadequacies in diagnostics or pain intensity scales? Diagnosis is not a purpose of everyday life, and diagnostic measures are not products of everyday theory. Similarly, pain intensity scales are not everyday products: they are products of specialised, scientific inquiry. Even if it is granted that these metrics are overly simplistic, how is our everyday notion or its use in everyday discourse thereby inadequate? Simplistic intensity metrics, she claims, are inadequate. Inadequate for what? Presumably, to capture pain as (alternatively, then) posited by our everyday theory.15 It is using our everyday theory which allows us to see the inadequacies of diagnosis and treatment. Hardcastle is certainly right that overly simplistic metrics and illegitimately shoehorning pain into a unified diagnostic category can wreak havoc for treatment. These are serious problems that need to be addressed. But diagnosis and pain metrics are not part of everyday discourse, so whether they are adequate is not appropriately blamed on (or credited to) our everyday notion. While these problems may provide further reason to think that pain is an inadequate notion for specialised, scientific purposes, or that our metrics for testing and measuring pain in the clinic are inadequate, they provide no support for traditional

190  Rejecting Traditional Eliminativism eliminativism. Inadequacies in our specialised methods for diagnosing and testing pain do not show that there are no pains. In sum, while Hardcastle’s stated position is traditional eliminativism without scientific eliminativism, her arguments at best provide support for the latter view, while leaving our everyday notion of pain unscathed. Hardcastle has done the field a service by nudging theoretical, philosophical debates about the nature of pain deeper into the messy world of pain research. That is truly laudable. Based on this research, however, Hardcastle concludes that pain is a useful notion for scientific discourse while the everyday notion should be eliminated. The appropriate conclusions, however, are at best the opposite: she has provided reasons to worry about the adequacy of the notion of pain for specialised, scientific discourse, but none to worry about its adequacy in everyday life. We may grant her, like Dennett, that our everyday notion of pain has been discovered to be associated with the complex activity of multiple mechanisms, none of which well-correlate with that notion. We may also grant her that our diagnosis and treatment of pain conditions, including the use of pain metrics, are inadequate enough to raise suspicions that pain, as posited by the our everyday theory, is a useful or appropriate treatment target.16 Granting all this may provide further support for the idea that pain isn’t an appropriate object of scientific inquiry, but it doesn’t undermine the existence of pain. Put another way: further reasons for scientific eliminativism may be gleaned from Hardcastle’s work, but none of these reasons for scientific eliminativism are reasons in favour of traditional eliminativism. One may, however, hold that scientific eliminativism is itself an argument for traditional eliminativism. While Hardcastle allows that some of our everyday posits may be acceptable despite not being referenced in scientific inquiry, many others—including Dennett, as we’ve seen—do not. And as above, Hardcastle herself asserts that the inadequacies of our everyday theory of pain for diagnosis and treatment shift the burden of proof to the advocate of that theory. If scientific eliminativism for pain is granted, are we thereby forced to accept traditional eliminativism for pain? In the next section, I argue that we are not. The lack of scientific utility does not entail a lack of everyday utility or success. Our everyday notion of pain is useful for our everyday purposes. Despite the surprising discoveries of pain science, we can continue to accept the complex reality of pain.

5.4 From Scientific Eliminativism to Traditional Eliminativism Does scientific eliminativism entail traditional eliminativism? If ‘pain’ should be eliminated from scientific discourse, should we therefore eliminate it from everyday speech? I see no good reason to think so. We

Rejecting Traditional Eliminativism  191 should hang on to our everyday notions unless we have good reason to abandon them, and a lack of utility for scientific purposes, all by itself, is not a good enough reason. Instead, for evaluating our everyday posits we should look to their utility for our everyday purposes. And for everyday purposes, references to pain are useful. Accordingly, we should continue to accept such references as successful. To evaluate scientific eliminativism, I have argued, we should ask questions concerning scientific utility. So, of pain, we ask: is the kindterm (‘pain’) playing a useful role in the scientific discourse? Is it useful for scientific explanation and predication to refer to pain? Dennett, Hardcastle, and I have all given reason to think that the answers to these questions are negative. There are, that is, good reasons to think that reference to pain for scientific purposes is not useful and that such references should therefore be eliminated from scientific discourse. Eliminate references from science because they are not useful for science. To evaluate traditional eliminativism, I now submit, we should ask questions concerning everyday utility. So, of pain, we ask: is the kind-term (‘pain’) playing a useful role in everyday discourse? Is it useful for everyday explanation and prediction to refer to pain? Nothing in Dennett, Hardcastle, nor I are good reasons to think that the answers to these questions are negative. And indeed, I don’t think there are any. There are, that is, no good reasons to think that reference to pain for everyday purposes is not useful and, accordingly, that such references should be eliminated from everyday discourse. We should only eliminate references from everyday life if the references are not useful for everyday life. Focussing on utility in this way allows us to see how reference to some things may be useful for some purposes, though not for others. Pain, or any other posit of our everyday theory, may usefully receive reference for the purposes of our everyday life, even if it is not usefully referenced for any scientific inquiry. This need not trouble us if we attend to the fact that the purposes of the folk are not entirely the same as the purposes of the scientist. Whether a posit is useful for folk purposes is not appropriately evaluated based on its utility for scientific purposes. Accordingly, we may grant that pain neither admits of mechanistic explanation nor is otherwise usefully referenced for scientific discourse, while maintaining that the utility of reference to pain for everyday purposes is left untouched. But are references to pain useful for everyday life? I have been assuming that they are and that failing to be useful for scientific inquiry doesn’t undermine this. What are the everyday purposes for which referring to pain is useful? It is now time to rehearse some mundane and obvious truths. Pain is a posit of our everyday theory that it is usefully referenced for a wide range of everyday explanations and predictions in everyday life. ‘Pain’ is canonically used to refer to those episodes which

192  Rejecting Traditional Eliminativism paradigmatically—if not necessarily—include characteristic sensations, perceptions, emotions, and avoidance behaviours. This everyday notion of pain is useful for communicating with each other in our everyday lives. When I say I am in pain, I tell you something. Indeed, I can lie to you and say that I am in pain when I am not. Our everyday posit of pain facilitates self-identification, self-ascription, and communication to others about the bad things happening to us presently—both to our bodies, as in “physical pain”, and to our minds, as in the so-called “mental pain”. It is instrumental in our search for medical attention, compassion, and sympathy. It facilitates our ability to protect injured limbs, to limit how far we push our bodies, and to identify potentially toxic chemicals and stimulation. We usefully refer to pain with lamentable frequency. It is, I suspect, the very promiscuity of our everyday notion that lends it so much utility in our everyday interactions and in our self-monitoring. We usefully speak of emotional pain, physical pain, stinging or throbbing pain, growing pains, and fiscal pain—even pains that do not bother us. As argued in Chapter 2: woe betide the philosopher who attempts to claim that some single or clustering of the paradigmatic features of this diverse class of episodes are necessary, sufficient, or essential to pain as referenced in our everyday lives—at least, if they are trying to capture the everyday notion of everyday people as they reference pain in their everyday lives. In everyday life, we accept a wide and diverse range of things as pains and usefully reference a wide and diverse range of things to explain and predict each other’s behaviour in a wide and diverse range of circumstances. As we’ve seen, however, the promiscuity of our everyday notion of pain may also contribute to its lack of utility for specialised inquiry. In particular, I argued that the complex idiosyncrasy of pain, as accepted by our everyday theory, undermines its utility for scientific inquiry, which aims at generalisations. So too, our everyday descriptions of pain may well fail to supply useful or appropriate categories for medical diagnosis, as emphasised by Hardcastle. Nonetheless, our everyday descriptions of our pains—while quick, loose, and diverse—are often extremely useful for, e.g., getting us to a doctor and getting a doctor’s attention.17 Given these many uses of our everyday notion of pain, we ought to continue to embrace it, even if it should be eliminated from scientific discourse. As above, none of the utility for everyday life is lost by establishing a lack of utility for scientific discourse. And the everyday utility is plentiful and manifest. This is not to say that our everyday notion of pain is incontestably sacrosanct. Advancement may yet undermine or supplant it. It may turn out, as it always may, that we are wrong. It may turn out that there are no pains after all and that the purposes identified above, and many more unmentioned, would be better served through elimination of any references to pain. Science may sometimes overturn our everyday posits:

Rejecting Traditional Eliminativism  193 as, arguably, with witches, ghosts, or goblins. I deny, however, that any of the reasons currently on offer for thinking that pain is not usefully referenced for scientific inquiry are good reasons for thinking that it isn’t usefully referenced for everyday discourse. Let us grant Dennett that pain will not submit to a mechanistic explanation. Indeed, I have argued for this myself in Chapter 3, on other grounds. That lack does nothing to undermine that I may usefully communicate something by expressing and reporting my pain. The pain that I am experiencing, here and now, may not be explained by the activity of any one mechanism, but instead by the activity of multiple mechanisms. These mechanisms may dissociate in ways that confound correlations between pain and mechanistic activity that is adequate to support scientific discourse. All of this we may (and indeed, I think we should) grant Dennett. None of this undermines that I, here and now, have a pain and that it may be useful for me to identify, express, and report it. My own argument in Chapter 4 was that reference to pain should be eliminated from scientific inquiry because pains are the result of complex idiosyncratic mechanistic convergence, and that this complex idiosyncrasy undermines useful scientific generalisations about pain or pain types. This complex idiosyncrasy, however, does nothing to undermine any of the everyday purposes identified above. Each pain is explained by the idiosyncratic convergence of multiple mechanisms. This is surprising. But that my pain right now has an idiosyncratic explanation does not undermine that I have usefully communicated something to you about my current situation by referencing it. Everyday theory, unlike scientific inquiry, happily embraces and accommodates idiosyncrasy. I bring my mother a mug of peppermint tea when she has a headache, I pour my best friend a stiff martini for hers, and I myself plump for sparkling water. I can reliably predict that taking a sarcastic tone will delight my husband and perturb my grandmother. I explain the doodling behaviour of my head of subject in the staff meeting one way (he is concentrating) and my own another (I am suppressing frustration). This sort of idiosyncratic complexity is rife throughout our everyday theory—and we easily accommodate it for our everyday purposes. Our everyday posits are, it seems to me, constantly tailored to the idiosyncrasies of the person whose behaviour we are explaining or predicting by attributing them. I am claiming that scientific eliminativism of something provides no reason, by itself, to revise our everyday theory about that something. I am denying, that is, that non-naturalness entails non-existence. Though this is not a move that Hardcastle makes, we’ve seen it to be a move of Dennett’s. Indeed, it is a rather common move in the current climate. One may think that scientific inquiry is the final arbiter of what exists, such that if something is not usefully referenced for scientific inquiry, then we ought to conclude that it doesn’t exist.

194  Rejecting Traditional Eliminativism To be perfectly blunt: I see no reason to accept that science is the only or final authority on what exists. While this is a big claim that I cannot fully address here, there is space to notice that many examples support rejecting it. Consider, for example, the days of the week. Tuesdays, I take it, are not usefully referenced in the generalisations of any science. Let us imagine, as seems plausible, that this would remain the case in an idealised, fully mature science. If ‘Tuesday’ does not usefully appear in our completed scientific discourse, should we conclude that Tuesdays do not exist? This is a big question and, for now, I am happy to conclude that the ontological status of pains is as robust as that of Tuesdays. One may say that there are not really any Tuesdays if they like, but Tuesdays are real enough for me and for my everyday purposes. Similarly, one may say that there are not really any pains if they like, but pains are real enough for me and for my everyday purposes. Denying that anything which isn’t usefully referenced for scientific inquiry doesn’t really exist, however, seems to me unmotivated and unnecessarily extreme. It should, of course, be admitted that Tuesdays and pains are arguably different in ways germane. In particular, pains are posits of our everyday theory that we take to have a functional, or causal, role. As introductorily noted, we say that pains are caused by things and that they cause things. We do not hold that Tuesdays are caused or caused things; e.g. Tuesdays follow Mondays but Mondays don’t cause Tuesdays to come into existence. One might reject the idea that only things which are usefully referenced in science exist, but hold on to the slightly weaker idea that anything which is posited as a part of the causal structure of the world only exists if it is usefully referenced by science. Science might not be the final authority on existence, but it may be the final authority on the existence of all the things which cause or are caused. Pain is indeed such a posit: according to our everyday theory, pain causes things and is caused by things. So, perhaps though Tuesdays may be real despite being non-natural, pains are only real if they are natural. This, too, seems to me unmotivated and unnecessarily extreme. And again, consideration of examples supports rejecting it. Consider, for example, friends. We successfully refer to friends in everyday discourse. When I call someone my friend, I say something meaningful, and I can lie and say that someone is my friend when they are not. Indeed, I can be wrong about who my friends are. Arguably, however, friendships—like we are claiming of pain experiences—do not admit of mechanistic explanations. Instead, whether someone is a friend at least seems to be explained by the complex convergence of many idiosyncratic factors. If friends have complex idiosyncratic explanations, then scientific generalisations about friends as such will be rather poor.

Rejecting Traditional Eliminativism  195 Let us imagine that it turns out that friends are indeed not a useful kind for scientific discourse and that we therefore shouldn’t refer to friends for any scientific inquiry. Friends, we discover, are not natural kinds. Nonetheless, of course, friends not only exist, but are a real and important phenomenon in our everyday lives. Scientific eliminativism about friends would not, by itself, entail traditional eliminativism about friends. It seems to me that this would remain so despite the fact that friends are posited as being part of the causal structure of the world. According to our everyday theory: there is a causal story about how someone becomes a friend, the fact that you are my friend causes me to do things, and so on. While more could be said about this example, I am again happy for now to conclude that the ontological status of pains is as robust as that of friends. I usefully talk about Tuesdays, friends, and pains in my daily life. I refer to them when offering successful explanations and predictions when going about my everyday purposes. Lack of utility within scientific discourse is irrelevant to these claims. The lack of utility for scientific inquiry does not by itself entail a lack of utility for daily life or that the posit of everyday life does not exist. As a final analogy, consider that something not usefully referenced in one science may nonetheless be usefully referenced in another. That something is not useful for chemistry does not by itself entail that it is not useful for biology. If something is usefully referenced for explaining and predicting, in any domain, that is a sufficient reason to continue to reference it within that domain. We should only eliminate references from a discourse because references are not useful for that discourse. This is as true when evaluating utility for one science and another, as it is for evaluating utility for science and everyday life.18 In light of the advances in pain science canvassed in previous chapters, the fact that we can independently evaluate references to pain for scientific and everyday purposes is good news. It was their laudable familiarity with pain science that caused Dennett and Hardcastle to become understandably suspicious about pain. Pain scientists no longer think that there is a pain mechanism and there appears not to be a valid biological marker for pain that corresponds to pain reports. The largest and most influential international, multidisciplinary body of pain scientists has declared that pains are whatever people subjectively report them to be. Pain eliminativists are right that reference to pain should be eliminated from scientific inquiry. It is then good news that accepting this does not entail accepting that pains do not exist—since references to pain are useful for everyday life. Indeed, references to pain are sometimes crucial in a wide range of high-stakes situations. Even if we grant scientific eliminativism for pain, we can rightly reject traditional eliminativism for pain. Advances in pain science make the former position increasingly plausible, while the latter position remains incredible.

196  Rejecting Traditional Eliminativism

5.5 Conclusion Pain is a posit of our everyday theory which earns its keep by its utility for explanation and prediction in our everyday lives. As it turns out, however, pains are complex and idiosyncratic such that they are not usefully referenced for scientific explanation and prediction. These scientific advances concerning pain may understandably raise concerns about whether we should continue to accept its existence. In this section, I’ve tried to alleviate those concerns. While the complex idiosyncrasy of pain undermines the utility of referencing it for scientific inquiry, it does not undermine the successful and useful reference to pain for everyday life. Pains are complex and idiosyncratic, but they are real for all that. Though these conclusions are significant, they prompt many questions which remain. Some are broad and general methodological questions. What are the implications for naturalism, for example, if we accept that some non-natural kinds, like pains, have existing members? While it may be okay if some of the posits of our everyday theory are non-natural (like friends and pains), do the foregoing considerations apply to all the posits of our everyday theory? Would it be a problem if they did? Particular questions about pain also remain. Accepting scientific eliminativism for pain and rejecting traditional eliminativism for pain, for example, raises questions about the status of pain in areas of life which are not obviously exclusively part of either everyday life or scientific inquiry. In particular, what do the foregoing conclusions entail about reference to pain for the practice of medicine or treatment for pain? Similarly, we might wonder what they entail about philosophical theorising about pain. I began this book by noting that our everyday theory of pain raises questions about the nature of pain that everyday theory alone can’t answer. But it may seem that I have yet to answer them either. If so, that’s surely unsatisfactory. While I won’t able to here provide complete answers to all the questions which may linger, in the next and concluding chapter I’ll at least gesture in the direction of what I think are the best answers to some of the most immediate questions prompted by the rest of this book. Much work will remain to be done.

Notes

Rejecting Traditional Eliminativism  197 The idea that a further label is needed seems to me to suggest that rejecting traditional eliminativism and being a realist about something—that is, holding that that something exists—implies that one is not a scientific eliminativist about it; or else, why need a further label to clarify that one is? That said, if one wants to emphasise that one holds that something is real (that is, one is not a traditional eliminativist about it) but not usefully referenced for scientific inquiry (that is, one is nonetheless a scientific eliminativist about it), then I suggest the moniker ‘everyday realism’ about that something. Using this term: I am an everyday realist about pain and take this chapter to argue for everyday realism about pain. As part of the very argument for this position is that realism has no commitments beyond what is in this endnote called “everyday realism”, I continue to refrain from using this term in the text.









198  Rejecting Traditional Eliminativism too, may be argued to be inadequate, this charge likewise leaves our everyday notion of pain untouched.

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6

Conclusion Living with the Complex Reality of Pain

6.1 Where We Have Been and Have Arrived 6.1.1 So, What Is Pain? Pains are a broad and diverse range of episodes with a number of paradigmatic features. A paradigmatic pain is undergone by a person who is aware that they are undergoing such an episode. A paradigmatic pain includes bodily damage and the perception of that damage. Such a pain is unpleasant for the person who undergoes it and is caused by something threatening that the paradigmatically pained, and indeed others, can recognise to have caused it. The paradigmatically pained will be motivated to do something about the unpleasantness, the damage, and their causes. When undergoing a paradigmatic pain, a person will be distracted and uneasy. A paradigmatic pain is expressed in behaviour, e.g. wincing, recoiling, crying, or cursing. These are some of the many features of a paradigmatic pain; that is, an episode which roughly everyone would agree and recognise to be a pain episode in the course of everyday life. Pain, in short, is just as our everyday theory posits it to be. Nothing in the preceding pages has undermined any of our folk platitudes about pain. Those statements about pain which we take to be obviously true in our everyday lives and which we will take most anyone with whom we interact in our everyday lives to take to be obviously true have here been taken to in fact be true. What, we might then wonder, was the point of this book? In attempting to answer this question, let’s back up and review. As I began by noting, our everyday theory of pain cannot alone answer every question about the nature of pain which might be raised. It is, in this sense, limited. For one thing, everyday theory itself raises seeming puzzles about pain which the theory alone cannot answer. According to our everyday theory, pains are mental episodes: we say, ‘I have a terrible headache’ and expect to be understood. But according to our everyday theory, pains are also extra-mental episodes: we say, ‘There is a terrible pain in my stomach’ and expect not to be met with any confusion.

200  Conclusion But surely no one thing, we might think, can be both mental and extra-mental. This puzzle is the so-called paradox of pain. However we may settle this puzzle, limitations of our everyday theory for specifying the nature of pain will remain. If we decide, for instance, to resolve the puzzle in favour of the claim that pains are mental episodes, our everyday theory remains unable to settle which kind of mental episode it is: a sensation, a perception, an emotion, a judgement, or something else besides. Similar limitations afflict any resolution which favours taking all pains to be extra-mental episodes; our everyday theory does not deliver a ruling concerning which type of extra-mental episode, if any, pains may be: a bodily disturbance, tissue damage, chemical signalling of some sort, or something else entirely.1 The folk platitudes of everyday theory enshrine a range of features which a paradigmatic pain will have, but everyday theory does not require—and indeed eschews—specifying more exacting criteria for whether something is a pain. As we noted, these limitations of our everyday theory are, to some extent, built in. The folk platitudes are statements about what’s typical and allow us to identify paradigms. Claims about what’s necessary, sufficient, or essential go beyond everyday theory. None of pains’ paradigmatic features are necessary or essential to pain as posited by our everyday theory: for each of the paradigmatic features of pains, there are some episodes which lack that feature, but which everyday theory nonetheless does not exclude. Similarly, none of these paradigmatic features are sufficient for pain: for each of the paradigmatic features of pain, there are some episodes which have that feature, but which everyday theory nevertheless does not include. And there are, of course, a host of controversial cases: episodes which have some paradigmatic features of pain but lack others, and about which we would not expect general agreement with everyone with whom we may interact in the course of our everyday lives. We might well have thought that an appropriate response to the limitations of our everyday theory of pain was to develop a specialised theory. Specialised theories can and should “clean up” our everyday theory; they aim at some further regimentations suitable for some further specialised purpose. Beginning with our broad and diverse everyday theory— and since pain is originally a posit of that theory, where else could specialised theorising begin?—a specialised theorist will aim to provide more restrictive criteria for when something is or isn’t a pain, answer the questions about pain’s nature relevant to that specialised inquiry, and offer solutions to the seeming puzzles about pain raised by everyday theory. In general, we might expect a (completed) specialised theory to offer answers to all questions about the nature of pain—at least, all those questions about the nature of pain which may be raised from the vantage point of that specialised theory type.

Conclusion  201 As seen in Chapter 2, here enters analytic philosophy. Contemporary, analytic philosophy of pain started with the assumption that pains are all and only those mental episodes with a distinctive qualitative character. This regimentation of our everyday theory has been taken as obvious—a place where contemporary, analytic philosophical theorising about pain begins. I thus dubbed this position the orthodoxy of simplicity. I also argued against it. I discussed why it seems to me that pains vary in their affective and sensory qualitative characters, challenging the idea that there is any further and supposedly distinctive qualitative character common and distinctive to all pain. Most centrally in this chapter, I also focussed on the failure of the leading philosophical accounts of this supposedly distinctive qualitative character. Ultimately, it is facts about the diversity of pain which undermines both representational and imperatival accounts in particular. Both what causes pain and what pains cause are massively heterogeneous such that pain is too poorly correlated with either for these theories to be credible. I then turned to another domain of specialised theorising: pain science. We might have thought that one result from turning to pain science to provide a more regimented, specialised theory of pain would be the identification of a pain mechanism or system—at least in the fullness of time. The identification of such a system may likewise have been expected to vindicate the orthodoxy of simplicity: perhaps pains are all and only those mental episodes with a quality that is well-correlated with the workings of such a system. Armed with the identification of such a system, perhaps we could dismiss the diverse range of causes and consequences of pain as misrepresentations or some kind of maladaptation; any such pains may be explicable through the workings of the pain system as malfunctions, false positives, or some similarly intelligible and natural phenomenon. Philosophical theorising and the orthodoxy of simplicity entirely aside, we might more generally have thought that identification of the pain system would allow us to regiment our everyday theory and answer any further questions about the nature of pain. As we learned in Chapter 3, however, the deliverance of pain science is instead that there is no pain mechanism or system. Each pain is, instead, the result of the idiosyncratic convergence of the activity of multiple mechanisms. While many have assumed that there simply must be some pain system which science would eventually uncover, as we’ve gone looking and actually carried out such scientific investigations, we’ve instead found other mechanisms—any of which may or may not be partially determinate of a pain. Surely, we might nonetheless have thought, pain science remains the right specialised theory towards which to turn: isn’t there some useful scientific regimentation of our everyday theory? We might have thought

202  Conclusion we must surely be able to have a science within which pain is usefully referenced for explanation and prediction. Pains must be natural kinds of some sort or other, or if pains as such are not, then at least more specific types of pain must surely be. Given that pains exist, we must surely be able to deploy specialised scientific theorising to unlock the secrets of their nature. As I argued in Chapter 4, however, neither pain nor pain types are usefully referenced for scientific explanation and prediction. The complex idiosyncrasy of pain, discovered upon our search for a pain system or mechanism, undermines the success of scientific generalisations—and science is in the business of offering generalisations. Rather than retain generalisation about pain or pain types, we should, for the specialised inquiry of science, replace these with references to mechanisms as appropriate on a case-by-case basis. If we do this, then far from losing utility, our scientific explanations and predictions will improve. The complex idiosyncrasy of particular pains is such that scientific generalisations about pain types or pain as such are inevitably less successful for explanation and prediction than generalisations about mechanisms which are relevant in any particular case. Science is thus not a specialised theory which can usefully regiment our everyday theory and limn the nature of pain. On the contrary, we should eliminate references to pain from scientific discourse. If these conclusions are correct, however, then should we begin to doubt that pains exist at all? Isn’t science our ultimate authority on questions of existence? If pain is not natural, doesn’t this suggest that it isn’t anything at all? If we should eliminate references to pain from scientific discourse, should we also eliminate references to pain from everyday discourse? Notice too that if we simply reject the existence of pain, then the pesky questions about its nature with which we began need no longer trouble us. Like witches and goblins, perhaps our everyday theory was simply wrong about whether there are any pains. We no longer trouble ourselves about the metaphysics of witches. Perhaps pain puzzles may similarly be solved by denying that there are any. As discussed in Chapter 5, however, we can and should continue to accept the reality of pain. While the complex idiosyncrasy of pain undermines the utility of referencing it for scientific inquiry, this same complex idiosyncrasy does nothing to undermine the utility of referring to it for everyday life. Though we should eliminate reference to pain from our specialised scientific inquiry, reference to it in our everyday lives remains useful for our everyday purposes. In our everyday life, we can and do respect the complex idiosyncrasy of the people and pains we encounter, even if complex idiosyncrasy is inevitably—and appropriately—lost for scientific generalisations. Though we have in this way returned to everyday theory, the exploration of this book has not been futile. Some conclusions are negative.

Conclusion  203 There is no pain mechanism or system. Neither pain nor any type of pain is a natural kind. The orthodoxy of simplicity should be rejected. Other conclusions, however, are positive. Pains are complex: each involves the activity of multiple mechanisms, none of which are specific to pain. Pains are idiosyncratic: the convergence of activity which determines each pain varies non-negligibly from person to person and for the same person across time. Pains are real: they are usefully and successfully referenced in everyday life. One might remain concerned that these conclusions fail to address the limitations of our everyday theory. Our consideration of scientific and philosophical theories of pain has illuminated hidden and surprising features of pain, but we are nonetheless apparently left without any regimentation that solves the seeming puzzles with which we began. I have offered no account of the essence of pain. There is no identification of the necessary or sufficient conditions for when something is a pain. In response, I suggest that in attempting to regiment our everyday theory for specialised purposes, we have overlooked the very core of its utility for our everyday lives. Each token pain, we have learned, results from the idiosyncratic convergence of the activity of multiple mechanisms. Accepting that pains are a broad and diverse class characterised by paradigmatic features, none of which are necessary and sufficient for pain—as our everyday theory does—allows us to respect this complex idiosyncrasy. The promiscuity of our everyday posit makes that posit better suited to play its well-accepted role in our everyday lives as we go about our everyday purposes. A role that is not only well accepted, but extremely useful. What I am suggesting is that the ‘limitations’ of our everyday theory are a feature and not a bug. They are not problems to be solved. Regimentation is not required. For everyday purposes, for example, we recognise that pains paradigmatically involve both a way that we, as people, feel and a disturbance in some part of our bodies. There is no need, for these purposes, to declare that pains are not really located in our bodies or that they are not really felt by us as people. Yet less need we declare that pains are really sensations, perceptions, bodily commands, or any other particular type of mental episode. We need not render a verdict concerning whether they are really some particular type of bodily disturbance, tissue damage, chemical signalling, or any such thing. We needn’t declare that pains are essentially unpleasant, that they are essentially conscious, or that they are essentially anything else. We needn’t even hold that there is a particular pain system or mechanism or that they are scientific entities of any sort. Fetishism about essences is here (as elsewhere) unhelpful. For our everyday purposes, we needn’t regiment our theory in any of these ways. Granny’s references to pain are doing just fine—better than fine—for all of Granny’s everyday purposes.

204  Conclusion Not only do references to pain remain useful for our everyday purposes without our regimenting everyday theory, but in closing I suggest that deploying the resources of some specialised inquiry to restrictively regiment would result in our losing some of the utility of our promiscuous pain posit. Consider again the mundane everyday purposes mentioned throughout this book or the references to pain from your own everyday life. We do not quibble when a person reporting pain is apparently unmotivated to take any corresponding bodily directed action or when there is no tissue damage to the place where the pain is felt. We do not draw a strict line on the basis of which we insist that pains are had only either by people or in bodies. We do not insist that some nonparadigmatic pain is not a pain, nor do we balk when someone either feels pain on an occasion when we would not or fails to find relief from an intervention which we typically find potent. Or at least, we should not. We may, of course, disagree on rare occasions about a non-paradigmatic case. Nonetheless, I submit that disagreement in non-paradigmatic cases is not something which we should seek to resolve by offering further restrictive criteria to apply in all cases. Embracing a diverse range of episodes, complex and idiosyncratic, is useful for communicating the diverse range of bad things happening to us, getting us to a doctor, engendering compassion and sympathy, and more besides. It is useful without regimentation, and it seems to me that regimentation would restrict its utility. As an analogy, briefly consider the childhood words that we use to refer to pains, e.g. ‘owie’, ‘ouchie’, or ‘boo-boo’. Notice that we do not seek regimentation of the owie, ouchie, or boo-boo theory. We do not seek a specialised theory to deliver the necessary and sufficient conditions for boo-boos or ouchies. We do not seek a science of owies or reference them in our specialised theorising. Good thing too, as these posits are not amenable or aided by such inquiries. Specialised scientific purposes are not among those for which these things were posited. It is, for all that, useful for our children to have posits which encompass a wide and diverse range of conditions. To submit these posits to more specialised inquiries would, in an important sense, miss their point: it would overlook the promiscuity which crucially contributes to their utility. When a child will report an owie and what they will class as a boo-boo varies across them and for each one across time. And we, as adults receiving these reports, appropriately tolerate a wide range of diversity before we correct them. We may disagree about when to correct them, but this is not something we seek to resolve by adding further restrictive criteria, and—crucially—a wide and diverse range that embraces complex idiosyncrasy is accepted by roughly everyone. Furthermore, we tailor our understanding of these reports to the particular children we know. Owies and boo-boos are broad and coarse posits, meant for quick, dirty, and frequent idiosyncratic reference.

Conclusion  205 As with all analogies, this one eventually breaks down. Children become more sophisticated. New words replace the old, reports become more infrequent, and more ailments are borne in silence. Nonetheless, adult pain reports are as usefully promiscuous as children’s reports of owies, ouchies, and boo-boos—if expressed in language more grown-up. When I tell the doctor that I have a pain in my leg, I do much the same thing as when a child shows me their finger and tells me they have an ouchie. Throughout these pages and in our everyday lives we see that our everyday theory of pain is useful for our everyday purposes. We should evaluate our everyday theory and its posits by its utility for our everyday purposes. In closing, I am suggesting that restrictive regimentation is not only unnecessary for these purposes, but it is positively deleterious. Everyday theory and the everyday lives for which we deploy it, however, are not isolated from specialised theorising and specialised pursuits, and the conclusions about pain drawn here are not without implications for these. While more concerns than I can here assuage undoubtedly remain, in closing, I briefly acknowledge some of them by offering some truncated reflections on the implications of the foregoing for medicine, naturalism, and philosophy.

6.2 Implications for Medicine As noted many times throughout the previous chapters: for pain, treatment is the crucible for theory. Any implications of the foregoing for the treatment of pain are thus of primary significance. Crucially, it may also seem that the prioritising of treatment which has supposedly governed the discussion is in no little tension with the conclusions at which I have arrived. I have concluded that while pains are usefully and successfully referenced in everyday life, neither pain nor any type of pain is usefully referenced for scientific explanation and prediction. One might think, however, that medicine—at least good medicine—is a science. If it’s not useful to refer to pain for scientific inquiry, must we then conclude that we shouldn’t refer to pain in medical practice either? This kind of medical eliminativism seems not only absurd, but it would apparently have disastrous implications for treatment. Medical eliminativism for pain should be rejected. People engaging with medical professionals report pain and require treatment in response. Pain reports should not be dismissed on the grounds that they include reference to unscientific kinds. Neither, returning to our analogy, do we dismiss our children’s reports of owies on any such grounds. Pain is real and the clinician should respond to its report. It should, however, be admitted that even as I do not take pain to be a proper object of scientific inquiry, I do not take it to be an appropriate target for a medical intervention. Interventions appropriately target

206  Conclusion mechanisms. This is one among many ways in which good medicine is indeed good science. But pain, as we’ve seen, is not subject to mechanistic explanation or usefully referenced in scientific generalisations. It is thus not appropriately targeted for treatment. And it is here that medical eliminativism may appear inevitable. The tension arises because medicine is neither merely an everyday nor merely a scientific endeavour. Problematic consequences follow from trying to shoehorn medicine exclusively into either. Everyday theory, on its own, is inadequate for medical practice. We benefit from specialised expertise and theorising. Scientifically validated, evidence-based medical interventions should be wholeheartedly embraced. But specialised scientific theory is likewise, on its own, inadequate for the practice of medicine. One among many reasons this is so, is the very one we’ve been considering: complex and idiosyncratic episodes successfully posited by everyday theory must be recognised as real when reported and the clinician must address them. Medicine thus stands at the interface. Neither merely an everyday pursuit, nor a purely scientific endeavour, medical practice involves both. Since pain is real, clinicians should accept pain reports. Since pain is not natural, however, clinicians must not simply accept the pain reports as identifying an appropriate treatment target. Rather, as suggested now some time ago by Wall (1996), pain reports are to be taken as invitations to ask further questions which may uncover a treatment target. More specifically, I am recommending that the clinician take pain reports in everyday language, and use those pain reports to identify non-pain treatment targets concerning which we have usefully explanatory and predictive scientific generalisations. In this way, a good clinician is in ways germane a good translator. They must be “fluent” in both the posits of everyday theory and also the relevant scientific theories. Many of us have undoubtedly suffered the consequences of clinicians whose ability to engage with us using everyday theory is poor: such a clinician fails to understand the real, if complex and idiosyncratic, episodes which we report and for which we are seeking aid. So too, a clinician’s ignorance or incompetence concerning relevant scientific inquiries is problematic; scientific inquiry, among other benefits, yields the identification of novel interventions which may be appropriate in a particular case and, crucially, teaches us which are to be rejected. While opinions may differ about which competency is best prioritised—for the treatment of pain or any other ailment—we should all agree that the best clinician is one who listens and understands complex and idiosyncratic reports couched in everyday language, and uses them to identify appropriate treatment interventions which have been scientifically validated. While the clinician must thus indeed accept and respond to pain reports, they need not target pain for treatment. Again, a pain report is an

Conclusion  207 invitation to identify a treatment target, it isn’t the presentation of one. As such, whether and when to use particular pharmacological agents, e.g. morphine or other opiates, may be decided based upon the particular role of the particular mechanisms that the clinician hypothesises is being played in the case of a particular pain being reported by a particular patient. There is inevitably a lot of particularity here involved. The idea in a nutshell is that appropriate treatment in response to pain is targeted at the mechanisms most credibly taken to be most effectively targeted to relieve that particular person’s pain on that particular occasion. Sometimes what’s needed is a powerful drug. Sometimes it’s a surgery. Sometimes it’s a shoulder upon which to cry. Sometimes it’s a nap. A good doctor, as we might put it, tailors their treatment to their particular patient. Indeed, put this way, this implication for medicine has the ring of triviality. It is worth noting that nothing in this picture requires that the clinician accept pain reports as infallible or inerrant, any more than everyday theory requires that we accept one another’s pain reports as infallible or inerrant. This seems to me as it should be. The strange idea that we are infallible about our pain reports was offered by the IASP in the light of our failure to identify any biological marker for pain in the body. The medical community, in essence, threw up their hands and let pains be whatever anyone says they are: if pains weren’t scientific kinds, then anything anyone says goes. We are now hopefully in a position to see that these are not our only options. While everyday theory takes pains to be a broad and diverse class of episode with features none of which are necessary or sufficient, it is nonetheless not anything goes. If a child approaches me with a cheeky grin, and declares the ice cream dripping down their hand ‘an ouchie’, I’ll laugh. I may play the game and ‘kiss it and make it better’, but I won’t accept their report as a sincere ouchie report. Similarly, I may sometimes, in other circumstances, think my child is pretending to have an ouchie when they don’t. I get to know my child and judge case by case. So too, in their earliest infancy, they must learn to use the word ‘owies’ and ‘ouchie’ correctly. For them to learn, while they needn’t be given necessary and sufficient conditions (even implicitly), they must sometimes be corrected. Everyday theory doesn’t commit users to infallibility or inerrancy about anything. Of course, the history of medical practice is such that we have tended to commit the opposite error: we have rejected too many pain reports as mistaken for reasons which are themselves mistaken. From a historical perspective, we might then see the medical community’s decision to take pain reports as incorrigible and infallible as a kind of corrective. Children; women and minorities of other kinds; those suffering from chronic pain; and, in general, those reporting pains which didn’t fit the dominant scientific model of the day have all sometimes been rejected as mistaken or, worse, malingering. And with dire consequences for sufferers.

208  Conclusion As I hope is clear from the foregoing: we should on no account reject any pain reports as veridical for failing to correspond to the activity of any particular mechanisms or for failing to have any particular feature privileged by a specialised theorist, e.g. tissue damage at the place a pain is reported as being felt, motivation to take any particular type of action, or any other privileged feature. Nonetheless, however, it needn’t follow that we are inerrant or infallible about our pains. Insofar as this is a correction, it is an overcorrection. The overall picture is then as follows. One conclusion of this book is that each pain is the result of the idiosyncratic convergence of the activity of multiple mechanisms, such that pain is not subject to mechanistic explanations. Interventions, however, target mechanisms, and practitioners are appropriately tasked with identifying the best interventions. Patients requiring treatment, however, couch their reports in everyday language using everyday theory—including its posit of pain. To surmount this problem, practitioners must use claims about pain (and other everyday posits) to identify mechanisms which may be appropriately targeted with scientifically validated interventions. In this sense, the clinical practitioner may be seen as something of a translator: fluent in both everyday theory and its posits but also in the relevant scientific theories and its posits.

6.3 Implications for Naturalism One conclusion of this book is that pain is real, but not natural; that is, pains are successfully and usefully referenced in everyday life, but they are not usefully referenced for any scientific inquiry. One might worry that a nasty implication of accepting this conclusion is a nasty kind of non-naturalism. If pains aren’t natural, what kind of spooky, unscientific things are they supposed to be? This problematic implication may become yet more problematic when we consider whether the sorts of arguments offered against the naturalness of pain can be extended to other posits of our everyday theory. One might, that is, worry about the implications of the foregoing for thinking about the status of our everyday theory and its posits in general. Even if scientific eliminativism without traditional eliminativism is somehow acceptable for pain, is it an acceptable position for everyday theory as a whole? Do we really want to accept that everyday theory is a non-natural theory, but nevertheless successful? What kind of spooky, superstitious theory is it? In response, I emphasise that it is complex idiosyncrasy which renders pain non-natural. This complex idiosyncrasy we can and do respect and account for in daily life, but it is inevitably lost in scientific generalisations. Indeed, it is appropriately there lost: unlike the clinician, science neither does nor should care about the complex idiosyncrasies of particular individuals. Non-naturalism for complex and idiosyncratic features

Conclusion  209 of individuals arises, however, because such features exist whether scientific generalisations (can) capture them or not. This book has focussed on pain alone, and whether or not other of the posits of our everyday theory are likewise complex and idiosyncratic is something which must be considered on a case-by-case basis. My own suspicions are that at least many of them are. Given what I have said about how the promiscuity of the pain posit contributes to its utility for our everyday theory, this suspicion is perhaps unsurprising. For our everyday purposes, everyday theory does quite well. Moreover, for our everyday purposes, I can and should unproblematically adjust to the complex idiosyncrasies of the individual episodes of the particular individuals with whom I interact. In our everyday life, interacting with individuals as complex and idiosyncratic individuals is crucial for successful interaction. I know the ways in which my husband’s beliefs differ from my best friend’s, how their beliefs have changed over time, how both differ from my own, and I take all these differences into account when I interact with them—including when I engage in explaining or predicting their behaviour. The same applies to the other posits of our everyday theory and the other individuals with whom I interact. As we all know, some people are more adept than others at using everyday theory and adjusting to the complex idiosyncrasies of the individuals to whom its predicates apply. Some people, alas, are chronically interacting with others as if their mental lives are all the same—most annoyingly, as if other mental lives are all the same as their own. (Philosophers perhaps being lamentably among the worst offenders.) This is all quite reminiscent of what I have had to say about pain. Going one step further: even as adequately treating a person in response to a pain report requires identifying the particular mechanisms involved in the complex convergence which explains the particular pain, it may well be that adequately ‘intervening’ in response to beliefs, desires, pleasures, wishes, and so on may well require something quite similar. Effective intervention to change your particular desire may be most appropriately targeted at the mechanism(s) responsible for your particular desire on that particular occasion. This is merely a suggestion. And again, the posits of our everyday theory should be considered on a case-by-case basis. But I have my suspicions. That pain or other (or even all) of the posits of everyday theory is non-natural due to complex idiosyncrasy, however, need not and should not raise concerns that there is anything spooky or supernatural about them. As noted at the end of Chapter 3, a perfectly physical explanation of each token pain may, for all I’ve said here, be perfectly available. The same may be said, for all the conclusions of this book, about any or all of the posits of everyday theory. Again, the issue is simply that science doesn’t (and shouldn’t) care about the complex idiosyncratic posits of our everyday theory—physically realised or not. Complex idiosyncrasy isn’t spooky.

210  Conclusion In a similar vein, we might further worry about those ‘soft’ sciences which would perhaps seem to disintegrate if purged of any references to complex idiosyncratic entities. The issue here is more complicated. Insofar as such specialised purposes are scientific, then it seems to me that complex idiosyncrasy will inevitably appropriately fall away; giving way to generalisations and posits about which such generalisations may more successfully be proffered. This might prompt us to wonder whether at least some such ‘sciences’ are more like medicine—standing at the interface of everyday and scientific inquiries. Or, indeed, whether they are perhaps something else entirely. While I cannot fully settle this question here, in brief response I want to emphasise that while we have many useful, explanatory, and predictive theories and many of these are scientific, some of these may instead remain, to the end of days, usefully explanatory and predictive for only non-scientific purposes.2 Everyday life, I have been arguing, is one such purpose. It seems to me that we ought to consider whether the purposes of other specialised inquiries are scientific or not on a case-by-case basis. Literary criticism, for instance, while usefully explanatory and predictive for some purposes, does not at first blush seem to me to be usefully and explanatorily predictive for any scientific purposes. It is, it seems to me, not that sort of thing in part because it seems to me, like everyday theory, to be partially but ineliminably concerned with complex idiosyncrasies. What, then, about psychology? Or sociology? Or anthropology? I have my own suspicions about each, as I suspect will each reader. Ultimately, we ought to consider these on a case-by-case basis. The crucial point I want to make for present purposes, however, is that if these are not scientific, neither they nor their posits are thereby illegitimate. Regardless of the scientific status of any particular inquiry or area of inquiry, then, we can anyway confidently say that neither a theory nor its posits need be scientific or in this sense naturalised to be legitimate, useful, or acceptable. Seeking a unified, overall picture of the world—as we should—requires that we sometimes add, revise, and eliminate, so that all of our theories are consistent with each other. Each of our theories should inform and be consistent with the others. Why should we require, however, that a single discourse sovereignly describe everything? Why should we subjugate all theories and their purposes to a single theory and its purposes? It seems to me that we should not. Even as we do not require that every term useful for inquiries in biology is useful for inquiries in chemistry, so I am suggesting that we should not require that every term useful in everyday life, or any other specialised inquires, is useful for any scientific inquiry. The overall picture is then as follows. One conclusion of this book is that pain is real, but not natural. This conclusion implies that naturalism of a certain kind is false: namely, any version of naturalism which holds that any entities which are not scientific entities simply don’t exist. Tokens of a type posited by a theory—including and especially everyday

Conclusion  211 theory—may be real, physically realised, explanatorily and predictively referenced, and nonetheless fail to be usefully referenced in any scientific inquiry for any scientific purpose. Many other kinds of naturalism, however, remain available.3 One may, for instance, hold that all token entities are physical entities, and that the best test for successful reference is explanatory and predictive power. Insofar, then, as the conclusions of this book imply a kind of non-naturalism, the relevant kind of non-naturalism does not seem to me to be nasty.4

6.4 Implications for Philosophy As I’m an analytic philosopher, it’s worth finally offering some brief reflections on the implications of the foregoing for philosophy. As discussed at length in Chapter 2, the most dominant theories of pain from contemporary, analytic philosophy start from the orthodoxy of simplicity and attempt to provide a successful characterisation of the supposedly distinctive qualitative character in virtue of which a mental episode is a pain. I argued that not only were those particular dominant accounts problematic, but so too is the starting assumption itself. One might more generally wonder about the implications of the foregoing for any philosophical theory of pain which attempts to offer its necessary and sufficient conditions. One general implication is that this is a mug’s game: regimenting in this way, as I’ve claimed above, is a mistake that undermines the utility of the promiscuous pain posit for everyday purposes. Where, we might wonder, does this leave philosophy? Won’t a successful philosophical theory of pain identify the essence of pain? Isn’t philosophy in the business of providing necessary and sufficient conditions? Answers to these questions are controversial. The implications of the foregoing for the philosophy of pain plainly depend on what we think philosophy is in the business of doing. This, unfortunately, is not something about which even philosophers themselves agree. If we think that philosophy only properly identifies essences or necessary and sufficient conditions, then there is apparently nothing concerning pain for the philosopher to do. Pain is not usefully submitted to that kind of treatment (if anything is). So, on this view of philosophy, pain is not usefully submitted to philosophical treatment. As noted in the preface, however, my own view of philosophy is more expansive. Following Wilfrid Sellars (1963), I take philosophy to be concerned with how things, in the broadest possible sense, hang together, in the broadest possible sense. Indeed, it seems to me to be this grand generality which makes philosophy unique and distinctive (if anything does). In practice, this requires harmonising our many theories. Accordingly, in my own philosophical activity, I aim to understand how our everyday ways of understanding ourselves and the things we care about can be made compatible and continuous with our specialised theories

212  Conclusion from the humanities, science, medicine, and so on. As above, I do not take science to be the sole authority here, but instead to be one specialised purpose with which all the others need to be harmonised.5 On this view, the philosopher—like the clinician—is something of a translator. They must be fluent not only in everyday theory, but in those specialised theories which they are attempting to harmonise at any given time. The overarching goal is to develop an overall coherent and useful theory. The current work is hopefully an application of this methodology. I have here tried to harmonise specialised theories of pain from science, medicine, and philosophy to contribute to providing an overall picture that is coherent and useful. In everyday life, a broad range of episodes with a broad range of features are accepted as being pains. In science, pain is recognised to be complex with multiple dimensions, and is recognised to be poorly correlated with any identifiable biological marker in the body. In philosophy, overly simplistic theories or models of pain reign—maintaining that pains are all and only those mental episodes with some distinctive quality, with the other features of pain being relegated as mere causes or effects of pain. In medicine, the pain report is the only valid marker for pain: according to the IASP, pain is whatever you say it is. It is in trying to harmonise these that I have arrived at the view here presented. How well I have succeeded, I leave to the reader. However successful I have here been, if we think of philosophy as this expansive activity, there is surely much more to do. On this view, there is and will remain more philosophical work about pain to be done insofar as there is more to be done to determine how pain ‘hangs together’ with everything else. I have certainly not completed that task here.

6.5 Where Do We Go from Here? In defending our everyday theory of pain, it is true that we have in some ways simply returned to where we began. If the foregoing is correct, each token pain is the result of the idiosyncratic convergence of the activity of multiple mechanisms. I have argued that our everyday theory already respects this complex idiosyncrasy. ‘The end of all our exploring’ has thus indeed been ‘to arrive where we started’. But we should hopefully also, as the poet goes on to say, ‘know the place for the first time’.6 In going forward, it is my hope that our specialised theories of pain will begin to further appreciate and recognise its complex idiosyncrasy. I have above offered some necessarily brief reflections about what this might look like. There are not only real and practical dangers in referring to pain as if it is more simplistic and less idiosyncratic than it is, but there are real and practical benefits from taking its complex idiosyncrasy seriously. Insofar as the rise of the modern pain clinic and improved palliative care places the needs of the idiosyncratic and complex individual at their centre, they are some evidence that progress in this direction is

Conclusion  213 being made. Progress which constitutes improved, if still woefully inadequate, treatment in response to pain reports. More generally, there is reason to be hopeful that we are, collectively and across the disciplines, moving away from overly simplistic, narrow, and generalised theories of pain. May this be so, and may the present work contribute to further movement in this direction.

Notes





References DeVries, W. A. (2014).Wilfrid Sellars. Routledge. Davidson, D. (1970). Mental events. Readings in Philosophy of Psychology,1, 107–119. Eliot, T. S. (1943).Little gidding (p. 216). London: Faber & Faber. Papineau, D.(2016). Naturalism. In The Stanford Encyclopedia of philosophy(Winter 2016 Edition), Edward N. Zalta(ed.).https://plato.stanford.edu/ archives/win2016/entries/naturalism/. Sellars, W. (1963). Philosophy and the scientific image of man. Science, Perception and Reality, 2, 35–78. Wall, P. D. (1996). Response to editorial by Anand and Craig. Pain, 67(1), 209.

Index

Aβ fibres 93; see also nociception Aα fibres 91–93, 99; see also nociception action 57–74, 109, 204, 208; bodilydirected 57–58, 60–72, 204; experience-directed 57, 62–63, 65–68, 70; other-directed 64–68, 70 acute pain 36, 99, 121–124, 132, 138 affect 34–36, 38, 39–41, 45–48, 53, 59, 65–66, 75; affective component of pain 16–17; see also qualitative character affective qualities see affect Anand, Kanwaljeet 162–164 Armstrong, David 43–47, 54, 75, 79 avoidance: behaviour 11, 63–64, 192 autonomic system 37, 39, 113 Aydede, Murat 76–77, 165–166 bare: bodily care 66–70 Bayne, Tim 184, 186 Bechtel, William 12, 13–14 belief 3–4, 12, 42–43, 56, 130, 180, 209; see also cognition bodily damage 45–46, 50, 64, 177, 199; see also bodily disturbance; nociception bodily disturbance 6, 45–48, 55, 74, 80, 200, 203; see also bodily damage bodily location: of pain 2, 3, 4, 6, 11, 45–46, 49, 53, 125–126, 165 bodily theories of pain 4–6, 30, 203 Boyd, Richard 10–11, 14 C-fibres 19, 92, 99–100, 128; see also nociception chronic pain 2, 35, 49, 52, 63, 66, 85, 115, 121–124, 127, 132, 154–155, 189, 207; see also neuropathic pain

cognition 16, 25, 88, 130, 133; cognitive component of pain 16, 98, 105, 106, 117, 130; see also belief consciousness 5, 24, 30–31, 36, 38, 56, 59, 79, 107, 182, 186–187, 203 Craig, A.D. ‘Bud’ 72, 88–89, 108–114, 117, 120, 129, 162–164 Craver, Carl 13–14 Cutter, Brian 46–48, 50–51 Dennett, Daniel 12, 176–184, 185–188, 190, 191, 193 Descartes, Renee 91, 137 desire 1, 3–4, 12, 42–43, 59, 66, 80, 209 diagnostics 17, 20, 10, 121, 124–125, 184, 189–190, 192 Disease model of pain see medical model of pain dissociation syndromes 36–37; lobotomy 35–36, 40, 78, 182; insensitivity to pain 37–39, 52; indifference to pain 35, 37–38; pain asymbolia 36–4, 66–69, 78, 165, 182 eliminativism: traditional 26, 174–177, 180–181, 183–184, 184–188, 190–196, 208; scientific eliminativism 26, 142–148, 149, 154–156, 157–160, 165–166, 168, 175–177, 190–196, 208; medical eliminativism 205–206 emotion 5, 6, 25, 36–37, 40, 88, 104, 161, 165, 192, 200; see also homeostatic emotion evaluation 7, 16, 74, 76, 97, 105; evaluative component of pain 16–17, 98, 117 evaluativism 46–55

216 Index everyday psychological theory 1, 42, 84–85, 151, 164, 170, 174–175, 178–181, 193–196, 199, 209; limitations 3–7, 21, 30, 39, 200–201, 210; and medical practice 22–24, 188–190, 205–208; of pain 1–8, 16–17, 34–35, 40–41, 45–46, 62, 64, 70, 74–75, 98, 105, 166, 179–184, 186–187, 193–196, 199–200, 211–213; regimenting 75–76, 201–202; revising 25, 40, 46, 75–77, 176–177, 181–184, 202–205 Fodor, Jerry 3 folk psychology see everyday psychological theory Fulkerson, Matthew 76–77 functionalism 12–13; homuncular functionalism 180; psychofunctionalism 76–77, 85 Gate control theory 16–17, 86, 87–104, 107, 108, 112, 115, 117–118, 134, 147, 160, 176 genetics 116, 130–134, 159, 166 Glennan, Stuart 13–14 grief 2, 40, 165 Grahek, Nikola 35 Hall, Richard 56–58 hallucination 45–46, 49–51 Hardcastle, Valerie 176–177, 184– 190, 191, 192, 193, 195 headache 23, 48–49, 62, 63, 64, 66, 67, 69, 72, 85, 120, 121, 124, 132–133, 144, 154, 193, 199 homeostasis 108, 110–111, 114, 166; homeostatic emotion 108–109, 111, 112–114; homeostatic emotion theory of pain 108–114; homeostatic mechanism 10–12 hunger 61, 69–70, 84, 108, 111, 113 illusion 23, 44–45, 48–51 Imperativism 55–73 incorrigibility 161, 166, 182–183, 207; see also infallibility infallibility 166, 182–183, 207–208; see also incorrigibility inflammatory pain 99–100, 121–124, 132–133, 154–156 injury see bodily damage

intensity: intensity theory of pain 87–89, 160; of pain 1, 39, 46, 93, 101, 110, 118, 126, 132 intentionality 42–43, 55, 73; see also intentional content intentional content 32, 42–43, 50, 55, 56, 58–61, 73, 77; evaluative content 46, 79; imperative content 55–61, 71; indicative content 56; representational content 32, 44–45, 50–55, 58–60 International Association for the Study of Pain (IASP) 20–23, 26, 54, 148, 160–166, 207, 212 interoception 47, 53–54, 79–80, 110–112 introspection 32–33, 41, 60–62, 64–65, 70, 75, 97–98 intuition 35, 38–40, 59, 182–183 itch 6, 34, 44, 48, 55, 57–58, 61, 69, 70, 108, 109, 111, 113, 116 Klein, Colin 58–60, 61–62, 63, 64, 66–69, 70–73 Kripke, Saul 30–33, 39, 41, 42 labour: labour pain 52, 68, 174 Lewis, David 12–13 McGill Pain Questionnaire (MPQ) 33–35, 63, 197 mechanism: definitions of 13–14, 85–86; mechanism-based classification of pain 18–20, 126–129, 158; see also homeostatic mechanism medical model of pain 17–20, 126–128 Melzack, Ronald 16–17, 51, 52, 86, 87–104, 111, 115–118, 131, 147 mental qualities see qualitative character Merskey, Harold 162–164 modulation: 94–96, 129, 131 moods: grammatical moods 56–57 morphine see opioids, morphine motivation 7, 16, 17, 25, 46, 57–59, 62–64, 66–68, 72–74, 76, 97–98, 118, 177, 208; motivational component of pain 16, 98, 108–109, 117, 137; see also imperativism multiple realisability 12–13

Index  217 naturalism 26, 196, 205, 208–211 natural kinds 9–15, 24, 26, 85–87, 142, 146, 175, 183, 203 neuromatrix: neuromatrix theory of pain 115–119, 132 neuropathic pain: 18–20, 121–123, 128, 132, 156; see also chronic pain nocebo effect 130 nociception 6, 51, 112, 114, 185; nociceptors 6, 50–51, 91–93, 105, 112, 114, 161; see also C-fibres; Aβ fibres; Aα fibres nonsteroidal anti-inflammatory drugs (NSAIDS): aspirin 4, 21, 68, 122, 132, 135, 138, 150, 154–156; Tylenol 57 noxious stimulation 38, 51, 95, 111, 132 opioids 95, 127, 133; morphine 2, 21, 47, 95, 150–152, 165, 182, 207 pain clinic 23, 134, 212 pain report 2, 6, 8, 18–22, 124–125, 161–164, 206–208, 209, 212 palliative care 15, 17 paradox of pain see the puzzle of pain perception 5–7, 25, 43, 44, 56–57, 76, 90, 100, 109–110, 114, 115, 129, 186, 192, 199, 200, 203; the perceptual theory of pain 5, 44–45 phantom limb 2, 49, 62, 66, 115 phenomenology 165, 185; phenomenological character (see qualitative character) phenomenological reflection 107; see also consciousness; qualitative character placebo effect 130 pluralism 15, 26, 146–149, 154–159, 166 Price, Donald D 86, 104–108, 111, 112, 131–132 Putnam, Hillary 12–13 the puzzle of pain 4–5, 90, 199–200 qualitative character 24–25, 30–34, 41–45, 47, 54–61, 69–70, 73–79, 88, 104–105, 165, 187, 201, 211

referred pain 49 representation 42–44, 48, 110, 111; representationalism for pain 44–47, 50–55, 58–60, 61–62, 71, 73, 74, 90, 201; representational theory of mind (RTM) 43–45, 50, 54; see also evaluativism; intentional content Saunders, Cicely 16 scientific utility criterion 9–16, 87, 141–142, 146, 168 Sellars, Wilfrid 211 somatosensation 104–105, 118; somatic perception theory of pain 104–108 specificity theories of pain 90–92, 93, 96, 100, 108–110 stomachache 33, 35, 69, 144 suffering 2, 16, 17, 35, 46, 48, 52, 92, 189, 207 tactition 54, 80; see also touch thirst 56, 61, 70, 111, 113 threat 66–69, 71–72, 80, 104–106, 111, 118, 124, 132, 153, 199 tissue damage 7, 17, 18, 46, 48–55, 90, 94–95, 161–162, 165, 200, 203–204, 208; see also bodily damage toothache 5, 60, 68, 72 total pain 16, 23, 97 transparency 59–61 touch 38, 51, 63, 95, 104, 110, 113, 116 Tye, Michael 46–47, 48, 50 unpleasant 1, 2, 4–5, 11, 16–17, 34–41, 45–47, 57, 59, 74, 76, 88, 104–105, 113, 118, 132, 150, 161, 165, 177, 199, 203; see also affect Wall, Patrick 16–17, 21–22, 51, 86–104, 107, 111, 124–125, 131–132, 147, 160–165, 206 Woolf, Clifford 18–19, 122–124, 126–128, 133, 158

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