2564606

Journal of Philosophy, Inc.
When a Pain is Not Author(s): Valerie Gray Hardcastle Source: The Journal of Philosophy, Vol. 94, No. 8 (Aug., 1997), pp. 381-409 Published by: Journal of Philosophy, Inc. Stable URL: http://www.jstor.org/stable/2564606 . Accessed: 13/08/2013 04:11
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THE JOURNAL OF PHILOSOPHY VOLUMEXCIV, NO. 8, AUGUST 1997
WHEN A PAIN IS NOT* Naturehas placed mankindunder the govetoment of two sovereignmasters,pain and pleasure. JeremyBentham
,r uch to my surprise,a recent reviewarticlelin neuroscience 1 began with the following quotation from Hilary Putnam: > > v s "The typical concerns of the Philosopher of Mind might be represented by three questions: (1) How do we know that other people have pains? (2) Are pains brain states?(3) What is the analysis of the concept pain?"Upon reflection, I decided that the quotation was entirely apt after all. Philosophers do take pain as their paradigmcase in quite a number of projects, and the fact remains that we do not knowexactlyhow pain processingworksin the brain, so there is lots of room for wild and rampant speculation. A little digging into the philosophical literatureuncovered a wide range of opinions and arguments regarding how we think about pain. Indeed, I daresayjust about every conceivable position is currently held todayby some leading thinker or other. (See table 1.) We find some philosophersand neurophysiologistsarguingthat pain is com- t
\/
* Earlierversions of this paper were presented to the Departrnentof Philosophy, VirginiaPolytechnicInstitute and State University,in 1995, and at the Society for Philosophyand Psychology1996 Annual Conference. My thanks to both audiences for their thoughtful and thought-provokingquestions. I am most especially indebted to PatrickCroskeIy,MarkGifford,George Graham,MarjorieGrene, Bob McCauly,and Harlan Miller, and to Daniel Dennett for his illuminating commentary. 1 A.V.Apkarian,aFunctionalImaging of Pain: New Insightsregarding the Role of the CerebralCortex in Human Pain Perception,"Seminars in theNeurosczences, VII (1995): 279_93. 0022-362X/97/9408/381-409 381 C)1997 TheJournal of Philosophy,Inc.
THEJOURNALOF PHILOSOPHY
382
Averill
Eliminativist Completely Objective

Lntnnsicto - palt of body Behavionst Functionalstate
PerCeptlon
| Churchland |
Newton
wsukheesr
Wittgenstein, Davis Lycan Shoemaker I Tye Graham
Relation Purely subjective |

Mysterious Nonmysterious
Conee Nelldn Kaufman
KriGke
Grahek I
Table 1. Possible philosophical positions regarding the nature of pain, with the names of a few of the more prominent adherents listed. See the footnotes for bibliographic information.2
pletely objective; it is either intrinsic to the injured body part, a functional state, a set of behavioral reactions, or a tpe of perception. We also find some philosophers and psychologistsarguing that pain is completely subjective;it is either essentiallyprivateand completely mysteriousor it does not correlatewith any biological mark2 References for worksnot discussed elsewhere in this article follow:E.W.Averill, Journal Southern Functionalism, the Absent Qualia Objection, and Eliminativism," (1990):449 67; P.S. Churchland, aConsciousness:The Transxxwrrs of Philosophy, LXIV (1983): 8S95; E. ConQXarterly, mutation of a Concept,"Pacifc Philosophical Studies,XLVI (1984): 23948; W.E. Dandy, nee, aA Defense of Pain," Philosophical xzvm(1933): 35741; L. Davis, aFunctionalism framJohnsHopEnsHospital, BuUetin XII (1982): 231-49; G. Graham and G.L. Studies, and Absent Q!lalia,"Philosophical Amcan Phibsophical Stephens, aAre01alia a Pain in the Neck for Functionalists?" Philos arterly, xxg (1985):7S80; RJ. Hall, aArePains NecessarilyUnpleasant?" XLIX (1989): 64S59; R. Kaufinan,Ys the Concept phyand Phenlogwcal Research, xxm(1985):279-83;S. Kripke, Journalof Philosophy, OfPain Incoherent?"Southern as It Is Ydentity and Necessity,"in T. Honderich and M. Burnyeat,eds., P2ulosophy (New York:Penguirl, 1979); W.G.Lycan, aForm,Function, and Feel,"this JOURNAL, xorvm,1 (Janry 1981): 2450; N. Nelkin, aPainand Pain Sensations,"this jouRPs NAL, IXXXIII, 3 (March 1986): 129-48, and fReconsidering Pain,"Philosophical (Cambridge:HaIvard, VII (1994): 32543; H. Putnam, RenellnngPhilosophy chology,
WHENPAINIS NOT
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ers but is completely nonmysterious.Finally,we find a few philosophers who disagreewith both conceptions and hold that pain is not a state at all; either it does not exist as we commonly conceive of it or it is an attitudinalrelation. Furthermore,each of these positions has become grist for someone's mill in arguing either that pain is a paradigminstance of a consciousnessstate or that pain is a special case and should not be included in any general theory of consciousness. We are left with severalsignificantquestions and puzzles. Among them are Putnam's. I do try to answer Putnam's three questions here, but I also want to do more than merely carve out my niche among the myriadof positions.I aim to offer a diagnosisfor whywe have so little agreement concerning the nature of our pain states.In brief, I believe that there are two reasons. First, for many philosophers, there is a basic failure to appreciate the fundamental complexityof our neuronal processing.This is the less interestingcause. Myclaim is that philosophersare enamoredwlth dissociationexperiments, but fail to understandtheir purpose, which is to individuate the component pieces of our larger systems.I argue that our pain sensory systemfunctions according to the same basic rules of all of our sensorysystems. Second, for many psychologists,neurophysiologists,and philosophers alike, there is an explicit or an implicit reliance on some sort of gate-controltheory of pain. Although theories of this ilk can account for several "low-level" puzzling cases involvingpain (why it is that stimulatingour nociceptorsunder certain conditions can alleviate pain instead of causingmore, for instance), they are notoriously vague when it comes to discussing the central gating mechanisms. This vagueness,I believe, obscuresthe fact that we actuallyhave two separatesystemsinvolvedin our perceptions of pain. One functions as a pain sensary system (PSS), quite analogous to our other sensory systems.The other-pain inhibatory system (PIS), which developed independentlyof our PSactively inhibitsits functioning. Differentiatingbetween the two systemshelps explain the remaining controversiessurroundingthe basic nature of pain. While a PSS
1992); S. Shoemaker, Functionalism and Qualia," PhilosophicalStudies, XXVII (1975): 291-315, Phenomenal Similaritnvr," Crztica, VII (1975): S37, and Absent Qualia Are Impossible,"Philosophical Rewew, xc (1981): 581-99;M. Tye, A Representational Theoxy of Pains and Their Phenomenal Character,"Philosophical Perspectives, sx(Atascadero, CA:Ridgeview,1995), and TenProblems of Consczousness: A Representational Theory of thePhenomenal Mind (Cambridge:MIT, 1995); K Wilkes, Physicalism (London: Routledge, 1977).
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supports a perceptual view of pain as a completely objective phenomenon, adding in a PIS (without explicitlyrecognizing that fact) accounts for the stronglysubjectiveaspectsof pain. I shall claim that a PSS functions according to the same basic rules of all of our sensory systemsand that, insofar as the pain systemis a simpler system than, say,vision or audition, it makes sense to take pain perception as a paradigminstance of a conscious experience. But insofar as we also have a PIS, pain also becomes a special case in our collection of conscious phenomena. Hence, contra Putnam,we should not be using the experience of pain as an intuitive and unproblematicexample of consciousness. As a final conclusion emerging from my understandingof pain, however,we shall see that the sensation of pain what most philosophers of mind focus upon as absolutely central to being in pain is neither a particularlyfundamental nor a particularlyimportant component of our pain processing. One current popular research question in the philosophy of mind is determining whether some philosophicalapproachor other (for example, identitytheory,functionalism, weak supervenience) can capture in an appropriateway what sensationsfeel like.If I am right about how we should understand pain, then the fervor devoted to this project might better be spent elsewhere, for what something is like becomes less important n exp alnlng our mlnc .
* * . j
I. THE COMPLEXITY OF OUR SENSORY SYSTEMS
Let me begin by outlining a few facts regarding our other sensory systems.I do this as a preliminaryto discussingpain not because we understand,say,visualprocessing,so much better than pain processing we do not but because many of the facts of perceptual processing regarded as commonplace (even among philosophers of mind) are the same sort of facts that seem to confuse philosophers and psychologists when theorizingabout pain. Our visualsystemis quite complex, spans manyareasin the brain, and is comprised of severalsubsystems whose interactionsremain a mystery.It is widelyknownthat different aspects of visualprocessing occur in different processing streams. For example, color is processed in intralaminar pathway, while motion is processed in the magnocellular.The auditorysystemworks in an analogous fashion (though the interactions of its subsystemsare not as mysterious). The medial superiorolive of our auditorysystemprobablycomputes sound location using interauraltime differences. The lateral superior olive, on the other hand, computes sound location by using differences in interauralfrequency.
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What is importantto notice is that it is quite all right for there to exist more than one processing stream in each modality.We might be mystifiedhow color getsjoined with shape and motion so that we But we are not have unified visualexperiences of particularobjects.3 confused about whether the neuronal paths involved in computing an object's color are visual, or whether computing interauraltime We are perfectlyhappyto have each modality differencesis auditory. be involvedin severalmaybe ultimatelyunrelated computations.We say (or, at least, I say) the partsof the brain that normallyrespond to impinging photons are part of the visualsystem,and the partsof the brain normallysensitiveto air compressiontrainsare part of the auditorysystem. Naturally, this is a gross oversimplification of how our sensory modalities are actually individuated: without unpacking what is unworkmeant by anormalfunctioning,"the definitions are virtually able. By way of partiallyrectifying this gloss, let me briefly touch upon the top-down and bottom-up investigativemethodologies in neuroscience (and in psychology,to some degree), for these analytic tools help disambiguatewhat counts as normal functioning. More importantly, they allow us to make claims about which computational algorithmsand cell assembliesare and are not included in our brainsystemsand subsystems to isolate the dissociation First,scientistsuse the method of double If we can get X to processingstreamsthat comprise our subsystems. occur without Y and also Y to occur without X then scientiststake this as grounds to claim that Xand Yfunction as independent units. For example, explicit priming tasksin psychologydemonstratethat we can record the meaning of a word or phrase without storing its syntax;implicit primingtasksshow that the syntaxof word or phrase can influence later linguisticprocessingwhile the meaning remains because we startwith a crude parsstrategy inert. I call this a topWown ing of our systemwritlarge (for example, linguisticprocessing) and then divide that systeminto its component pieces (syntacticprocessing, semantics).This method of investigationforms the backbone of functionaldecomposition. Daniel C. Dennett's4 to unite the various analysas Second, scientistsrely on a teleologzcal and sundry parts into wholes. Breaking down larger pieces into smaller ones is not enough to get the explanatoryjob done, espesee my for discussion, 3 This is knownas the bindingproblemin psychology; of Solutions,"Journal Neurobiological andPossible Problem Binding aPsychology's 6S90. Studies, I ( 1994): Consciousness . MIT,1987) (Cambridge: Stance Intentional 4 The
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ciallywhen severalof our systemsoverlapinside the head. Our brain houses lots of individualprocessors;knowingall the pieces does not identify the larger puzzles. Why do scientistsbelieve that color and motion processingbelong to the same systembut that echolocation belongs to somethingelse? This is not a trivialquestion since each of the subsystemsis (mainly) anatomicallyand physiologically distinct from the other, and since individualneurons do not know the sort of signal to which they are responding. The informationcontained in an atmospheric compression wave or a photon wave triplet is transmittedas electricaland chemical energy once one moves inside the body. Scientistsuse three converging strategiesto isolate and construct systemsfrom the component dissociablesubsystems. First,they look for correlationsbetween neural firing patternsand events in the external world, verymuch what Fred Dretskeshas in mind with his informationalsemantics.Neurophysiologists take the smallestpieces of the puzzles, usuallyindividual neurons, or the extracellularspaces around small groups of neurons, and record what they do under a varietyof circumstances. They conclude that our color and shape detectorsbelong togetherbecause they are activeunder similarcircumstances, namely, when the orgarlism's retinas are bombarded by photons. Auditorycells are active in different contexts. Luckilyfor the scientistsand their correlationproject, true polymodalcells are relatively rare. Second, scientists look at the neural connections fore and aft. Aside from knowinghow a cell resonateswith the environment,they also need to knowto what this cell is connected-where the information the cell lights up to goes-and what is connected to the cellhow it gets the informationto which it does respond. Determining the processingalgorithmof any cell group is not as easy as it might sound; it is not a matter of merely recording all the stimuli it likes and then deciding what all the stimuli have in common. As S. R. Lehky and T. R. Sejnowski6 remind us, even cells that we think we know well, such as D. H. Hubel and T. N. Weisel's7 simple edge detectors,might not be involvedin the computationswe think they are. It is entirely likely, given Lehky and Sejnowski'ssimulaiion results,
5 Knowledge and theF>w of Information (Cambridge:MIT, 1981), and Explaining Beha7xor: Reasons in a World of Gauses (Cambridge:M1T,1989). 6uNetwork Model of Shape-from-Shading: Neuron Function Arises from Both Receptiveand ProjectiveFields,"Nature, cccxxxm (1988): 452-54. 7 Functional Architectureof MacaqueMonkeyVisual Cortex,"Proceedings of the RoyalSocietyofLondanB,cxcvm (1977): 1-59.
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that the sowalled edge-detectorXcells actuallyare involvedin computing an object'saxes of curvature. Foranother,more striking example,considersynesthesia, a condition in whichone gets a bimodalexperiencefrom monomodalinputs-one can see and hear colors or tasteand hear words.8 Althoughwe would probably wantto saythatsomeoneseeing blue columnswhen she hears a bell ringing is havinga visualexperience,we would not want to say thatatmospheric compression wavesare visualinputs,even for this person. The inputs are still auditory; they come in through the ears and passthroughthe traditional auditory centers.Theyjust happen also to travelthroughsome of the visualpathways (probably via the limbicsystem). If we only had accessto single-cell recordingsof synesthetic cells, we would obviouslymisidentitr what those cells were doing. Knowing how thingsare connectedprevents us from leaping to whatwouldotherwisebe an entirely rational(butalsoentirelyfalse) conclusion. Finally, scientistsconsiderhistorical and evolutionaiyfactswhenever possible.We are biologicalorganismsequipped to move throughour environment.We evolvedthat waybecause (roughlyspeaking) those who can move most effectively through their environmentsucceed in reproducing the most.When thinkingaboutour perceptual systems, especially whenwonyingaboutvarious components'purposes, it is important to keep in mind how the hypothesized system or subsystemis supposedto functionwithregardto motorassembling. Formost if not all, information processing in the brainis relatedto the motorsystemin one wayor another.Forexample,the visualareasall haveat leastsome indirect contactwith some motor structureor other, either the basal ganglia,or the motorcortex,or the tectum,or something.9 Motorinformationneeds to be zsiphoned ofF the visualpathways at all stagesalong the ascendingroute so that the visualinput can be used for motoroutputl 01ite often what seems strangeor curiousfrom a psychological pointof viewseemsquitenatural froman evolutionary standpoint. If we can groupsubsystems togetherinto largersystems via theirfunction-which isjust whatit is aboutthat systemthat increases the reproductiverate of the organismthat houses itll then so much the better. The brain puts great emphasison the priorityof motor tasks,and we
8 R.E. Cytowic,Synesthesia: A Unionof theSenses(New York:Springer, 1989), and TheMan WhoTasted Shapes: A Bizarre Medical Mystery O2ers Revolutionaty Insightsinto Reasonin$ Emotion, and Consciousness (New York:Putnam, 1993). 9 E.R. Kandel and J.H. Schwartz,Prznciples of NeuralScience (New York:Elsevier, 1985, 2nd ed.). 10 P.S. Churchland, aEpistemologyin the Age of Neuroscience," this JOURNAL, IXXXIV, 10 (October 1987): 54453. " Cf. C. Wright,aFunctions," Philosophical Retnerv, Lxxxs (1973): 13932.
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should payattentionto this emphasis. Whatever purposewe ultimately proposehasto fitwithour biological natures.(Often,however, suchconsiderations are not possibleor are littlebetterthanjust-sostories,for the detailsof the advantages havebeen lost overevolutionary time.Whydo we see in color,for example? Whatreproductive advantage wouldit have givenour ancestors long ago?The answer is not easy,nor is it clear.) I call this collection of researchstrategiesbottom up because we begin with the smallestunits in the brain and then arrange them into nested hierarchies.Based on gross similaritiesin response patterns, connections to other systemsand organs, and putative selective advantages,we group the doubleZissociatedsubsystems into hierarchically arranged classes. The process is not cut and dried by any means, but it is the best we have at the moment. Perhaps someday we shall be able to identify definitivelyto which systemvariouscell assembliesbelong in virtue of the inherent rhythmsof the cells' firing patterns,or something like this.l2 Until then, though, the best we can do is to make educatedguessesbased on convergingevidence. Both approachesare required for a complete explanation of psychobiologicalphenomena. By breakingcognitive engines into interacting component pieces, the top down strategyhelps explain why organismsbehave the waythey do; and by categorizingand grouping the isolatedparts,the bottom-upstrategyhelps explain what purpose the analyzedbehaviorserves.Remindingourselvesthat we use both strategiesin understandingour neural systemswill rid us of the tendency to make our pain systeminto a cartoon;and reminding ourselves of biological heritage will aid in justifying a counterintuitive system that prevents our pains from occurring. Ultimately,I claim that our systemfor perceivingpain worksin exactlythe same fashion as our visualand auditorysystems:it is a complex systemwith dissociable subsystems. Furthermore,it is a systemthat appearsquite naturalwhen consideredagainstan evolutionary backdrop.
II. A SKETCH OF OUR PAINSYSTEM
The classicview of our basic pain systemis of two three-neuronsubsystems.ls (See figure 1.)14 Each subsystem has a set of neurons which
12R. Emmersdescribes modalityspecific firing patternsin
the thalamusin Pain:
A Spzk0Interoal(ided Messagein theBrain (NewYork:Raven, 1981).
13Even the classic story is becoming more complicated; see E.R. Kandel,J.H. Schwartz,and JJ. Jessel, Pnnciples of Neural Science (New York:Elsevier, 1995, 3rd ed.), chapter 27. 14 I owe this vision of the classic view to S.A. Cross's excellent review article, aPathophysiologyof Pain," Mayo CEnic Proceedings,LXIX (1994): 37543. See also Kandel and Schwartz; and P. Roland, zCorticalRepresentationof Pain," Trends in Neuroscience, xv (1992):S5.
WHENPAIN IS NOT
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Frontal Cortex
<
Somatosensory Cortex
1 | Reticular _ _ Formation
_ _
SurfaceXC /
fibers t
i]
A-a fibers
L<Dorsal
Horn
Figure 1. Diagram showing ourpainsensoxy system. Thefirstset of neuronstakein information fromthe peripheIy and then synapse witha secondset of neuronsin the dorsalhorn.Theseneuronsascend,some terminating in the reticular formation of the brainstem,otherstraveling to the thalamus. Axonsthatterrninate medially in the thalamus synapse witha thirdset of neurons thatproject to the frontal cortex. Thosewhichterminate laterally synapse withneurons thatproject to the somatosensoxy cortex.
resides in the dorsal root ganglion of the spinal column. These neurons extend their axons to whatevertissue they innervateand receive external input there. They also have a second axon that projects acrossto the dorsalhorn. The axon in the dorsalhorn connects with
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a second set of neurons housed in the dorsal horn whose axons run out of the spinal column and up to the thalamus.The third set of neurons projectsfrom the thalamusto the postcentralgyrus in the cerebralcortex. In 1911, H. Head and G. Holmesl5proposed a dual systemof aXerent projections in our pain sensory system:an epicritic system that processes informationregarding intensityand precise location, and a protopathic systemthat deliversthe actualpain sensations.Eighty-six years later, we still believe they were fundamentally correct.We now know that we have a gsensorydiscriminative" subsystemthat computes the location, intensity, duration, and nature (stabbing,burning, prickling) of the stimuli.This subsystemis subservedby the A-8 fibers. These mechanoreceptiveneurons are mylinated,so information can travelquite quicklyalong them (approximately 5-30 m/sec, as opposed to .5-2 m/sec for information traveling along unmylinated pathwaysl6).Consequently, they transmit what is known as first pain" or afastpain." The threshold for activationis constant from person to person (thresholdhere), and this subsystemremains active (assumingno other defects in the organism) only as long as the rawnerve endings are stimulated. We also have an aaffective-motivational" subsystemthat supports the unpleasantpart of painful sensations.This systemfeeds directly into our motor responsesystemsand is consideredto be phylogenetically older than other aspects of our multifacetedpain system.This polymodal subsystem begins with the well-known unmylinated C fibers. Once they are activated,they will continue to fire for some time, even after the noxious event has ceased. This subsystemgives rise to what is known as aslowpain"or asecond pain,"so-calledbecause this is what we feel second wheneverwe are injured a diffuse and persistentburningpain. When someone has chronic pain, a protractedsecond pain is whatis being referredto. Similarto the color and form processorsin the visualsystem,the A-a-fiber and C-fiberpathways remain largelysegregated.For example, generallyspeaking,they terminatein differentlayerson the dorsal horn. But there is more interaction than what we find in either the visual or auditorysystem.The dorsal horn contains widedynamic range(WDR) neurons that respond to both A-8 and C neurons, as well as to other peripheralstimuli.WDRneurons are also sensitiveto
zSensolyDisturbancesSom CerebralLesions,"Brain, xv (1911): 102-254. Information traveling at the slower speeds would take about 8 seconds to reach a horse's spinal column from its hoof.
15 16
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visceralstimuli. It is possible that referredand sympatheticpains depend upon this sort of visceral-somatic convergence.'7 Once pain informationexits the dorsalhorn, it travelseither to the reticularformationin the brain stem or to the thalamus.Laninae I and V projectto the lateralnuclei in the thalamus,'8 and laminaeI, V, and Vl projectto the medialnuclei. Each type of nuclei underwrites a differentsort of information; the lateralnuclei processdiscriminative information(fastpain), while the medial nuclei and reticularconnections process affective-motivational information(slow pain). The two thalamicstreamsremain separateon their trip to the cortex as well. Pain neuronsin the lateralnuclei synapsein the somatosensory cortex, which then can compute the location and characteristics of the pain; those in the medial nuclei synapsein the anteriorcingulategyrusin the frontallobe, whichfiguresin our emotionalreactionsto pain.The frontallobe (and its connections)processour actualsuffering.
III. PHILOSOPHSCS ERROR
Nowwe can see howand whyseveral philosophers are mistaken in their conclusionsthat thereare no such thingsas pains,l9 or thatpainsare located in our limbs,20 or that pains are purelysubjective,2' or that pains are reactive behaviors.22 Eachof these positionsidentifiespainwithone of the neuronalgroupswithinthe painsystem, whilefailingto recognize that our pain systemis complexand containsat leasta duality23 of suS
17 For contrar,vevidence, though, see G.D. Schott, aVisceralAfferents: Their Contribution to 'Sympathetic Dependent' Pain," Brain, CXVII (1994): 397413. Other neurons that show this sort of convergence are the nociceptive-specific" neurons in lamina I and the complex" neurons in laminaeVII and VIIIof the dorsal horn. The interaction of autonomic information with somatic appears to be quite common throughout our pain system. 18A.D. Craig,M.C. Bushnell, E-T.Zhang, and A. Blomqvist,A ThalamicNucleus Specific for Pain and TemperatureSensation,"Nature, CCCLXXII (1994): 77S73. 19 P.M. Churchland, Reduction, Qualia, and the Direct Introspection of Brain States,"this JOURNAL, XXXVIII, 1 (January 1985): 8-28; Dennett, aWhy You Can't Makea ComputerThat Feels Pain,"Synthese, xecDcvm (1978):449. 20D.M. Armstrong, TheNatureof Mind and OtherEssays (Ithaca:Cornell, 1981); N. Newton, On Viewing Pain as a SecondaryQuality,"Nous,xxn (1989): 56998; G. Pritcher, Pain Perception,"Philosophical R, LXXIX (1970): 36S93. 21 G.R. Gillett, aThe Neurophilosophy of Pain,"Phtlosophy, IXVI (1991): 191-206; N. Grahek, Objective and SubjectiveAspects of Pain," Philosophical Psychology, IV (1991): 24966; C. McGinn, TheSubjective V;icew (New York: Oxford,1983). 22 L. Wittgenstein, Philosophical Investigations, G.E.M. Anscombe, trans. (Cambridge: Blackwell,1953). 23 R. Melzack and P.D. Wall, Pain Mechanisms: A New Theory," Science, CL (1965): 971-79, and E.R. Hilgard and J.R. Hilgard, Hypnosisin theReliefof Pain (New York:Brunner/Mazel, 1994, rev. ed.) both argue that there are three components to pain processing:the discriminative, the affective-emotional, and the evaluative. I find little physiological evidence to support these claims. Here, I discuss only two components.
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systems,each of which processesa differentsort of information.(See figure 2.) In general, philosophersmake these mistakesbecause they misunderstandthe double dissociationmethodology.We can, either throughpurposefulinteiventionor accidentsof nature,dissociateour discriminativepain processing from our affective-motivational pain processing.Ingestion of morphine (or other opiates), lesions to the medial thalamus,and prefiontallobotomiesall resultin sensationsof pain withouta sense of sufferingand withoutproducingcharacteristic pain behaviors(wincing,moaning,complaining,and so on) (ibid.).In these cases, patientscan localizetheir pains but are not upset by the
Behaviorlst
I Frontal
Somatosensory
Functlonal St ate
SubJect
Thalamus
ive
Reticular Formation
Percept lon
Part of the Body

Dorsal Horn A-a f ibers
Figure 2. Part of the pain system identified with different philosophical views regarding the basic nature of pain. Most views identify pain with one subsystemor with one sort of neural processor.Two exceptions are functional state and perceptual views of pain, though perceptual views of pain often overlook or underestimate the motor component of pain processing.
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fact that they are in pain. We can also get reverseeffects,to a degree. Fentanylcauses one to react in pain, yet inhibits our discriminatoxy abilitiesfor the pain.24 Lesion studiesarldstudiesusing hemispherectomies show that even with the cortex completelymissing,we can still havea pain sensation; we simplylackfine localization and intensitydiscrimination.25 Patients with Parkinson'sdisease and Huntington's chorea often have pain sensationsbut are unable to indicate where theyfeel the pains.26 We also find instances of the pain centers in the thalamus and cortex being activated without corresponding activationsof A-dor C fibers ("nociception"). Fully 80% of lower back pain sufferers present no external or internal injury.27 Phantom limbs and phantom pains in phantom limbs are quite common experiences in new amputees.28Stimulating the medial periaqueductal gray region, tectum, or thalamus directly can also result in painful experiences.29 Finally, our emotional states heavily influence the degree of pain we feel, quite independent of actual injury. Indeed, psychogenic pains, pains without any corresponding injury or peripheral stimulation, have been documented for quite some
time.30
24 R.H. Gracely,R. Dubner, and P.A. McGrath,aFentanyl Reduces the Intensity of PainfulTooth Pulp Sensations:Controllingfor Detection of ActiveDrugs,"Anesthesia andAnalgesia, LXI (1982): 751-55. 25 KD. Davis, R.R. Tasker, Z.H.T. Kiss, W.D. Hutchison, and J.O. Dostrovsky, aVisceralPain Evoked by Thalamic Microstimulationin Humans,"Neuroreport, VI (1995): 369-74; L.A. French, S.N. Chou, andJ.L. Story, Clnical Orthopedics, X1VI (1966): 8S86; Head and Holmes; and Roland. 26 E.H. Chudler and W.K Dong, aThe Role of the Basal Gangliain Nociception and Pain,"Pain, LX (1995): O85. 27 Wall, Introduction," in Wall and Melzack, eds., Textbook of Pain (New York: ChurchillLivingstone,1989, 2nd ed.), pp. 1-18. 28 See discussion in Hilgard and Hilgard;T.S.Jensen and P. Rasmussen,Phantom Pain and Related Phenomena After Amputation,"in Wall and Melzack,eds., pp. 508-21. 29Davis et alia; KAo Keay,C.I. Clement, B. Owler, A. Depaulis, and R. Bandelr, aConvergenceof Deep Somatic and Visceral Nociceptive-Information onto a Discrete VentrolateralMidbrainPeriqueductalGrayRegion,"Neuroscience, LXI (1994): 727-32. 3R. Roy, aEngel's Pain-Prone Disorder Patient: 25 YearsAfter,"Psychotheraphy Psychosomatics, XLE (1985): 126-35.In Illustrations of theInfluence of theMind uponthe Bodyin Healthand Disease Designed toElucidate theImagination (Philadelphia:HenIy C. Lee's, 1884, 2nd ed.), D.H. Tuke reported the case of a butcher who got fouled up on a meat hook and appeared to be in agony. When examined by the local chemist, however, it was discovered that the meathook had only penetrated his jacket sleeve and, even though the butcher was screaming in aexcessivepain," he was completely unharmed (p. 168, as reported in A. Gamsa, She Role of Psychological Factors in Chronic Pain, I: A Half Centuryof Study,"Pain, LVII (1994): S 15).
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OF PHILOSOPHY THEJOURNAL
Correlatively, there are also examples of our peripheral pain being activatedwithout this information proceeding on processors to the thalamus or cortex. About 37% of emergency-roomvisitors Athletes and soldiers can feltno pain at the time of their injury.31 they have been sethough even pain, continueperforming free of to engage in what subjects some Hypnosis allows verelyinjured.32 Placein pain.33 being without wouldotherwise be painful activities enough, (Interestingly pain. bosare notoriouslyhelpful in relieving theyrelieve pain at half the rate of the real drug, regardlessof the Of course, some lesions to the thalsupposedstrengthof the drug.34) amusand cortex can result in the cessation of pain experiences, eventhough the peripheralneurons continue to operate normally. Each of these double dissociations, however, individuates neuonly withinour overarchingpain system. ronalgroups or subsystems I make this claim by analogy with our other perceptual systems. Blindsightpatients can discriminateshapes and figures they claim not to be able to see consciously.Sufferersof Anton's syndromeinsistthat they can see perfectlywell, even though they are completely blind and have severebilateraldamage to their visualassociationareas. No one uses these facts to argue, however,that vision does not exist, or that vision is located in our eyeballs,or that vision is purely We maynot know exactlywhat or that vision is behavioral. subjective, to say about blindsightor Anton's syndrome,but no one claimsthat blindsightis not a disorder of the visualsystemor that patientswith a visualexperience of some sort. Anton'ssyndromeare not ha^iing By misunderstandingwhat a perceptual system in the brain encompasses,many philosophers miss the boat regardingthe basic na ture and structure of pain. Double dissociation alone does not individuateour basic systems;that is used to isolate the subsystems that operate within the larger system.We then need to build our different systemsout of the component pieces. Teleological considerations help us to do so. To wit: the neurons in our pain system all
T.C. Ty, aAcutePain in an EmergencyClinic: Latency of (1982):3S Pain, xnr Related to Different Injuries," Patterns Descriptor Onset and 43. Expen32 H.K Beecher, aRelationship of Significance of Wound to the Pain oftheAmencanMedicalAssoczation,c (1956):1609-13. ence,"Journal that at 33 Evokedpotential recordings of painful stimuli under hypnosis indicates least activityin the frontal lobe is affected (Helen Crawford,personal conversation). 34FJ. Evans,aThe Placebo Response in Pain Reduction,"inJJ. Bonica, ed., InterYork:Raven, rr (New Volume on Pain, Advancesin Neurology, national Symposium 1974), pp. 289-96.
31 Melzack,Wall, and
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respond to roughlythe same sort of information;they increase their rate of firing in the presence of noxious stimuli on skin or deep organs. Moreover,the connection among the six-neurontract is a stable, common, and isolablepathway. Connections fore and aft show a stream of informationflowing from the nociceptors on the skin up through the cortex.33 Finally,a pain sensory system tied to the somatosensory processorsmakesgood evolutionarysense. As creatures eking out lives in a hostile environment,havinga systemwhich could warn us when damage occurred and which could force us to protect damaged parts until they healed would be tremendouslybeneficial. (Indeed, persons who cannot feel any pain at all often live a nasty, brutish,and short life.36) Neither our conscious experience of pain, the damaged tissue itself, nor our bodily or emotional reactionsare fundamentalto pain processing.Each is but one component of a largerprocessor.Hence, it is a mistaketo tryand claim one or the other as pain simpliciter. It is equallyerroneous to conclude that since we cannot identify one or the other with pain, there is no such thing. The entire pain sensory systemfunctionslargelythe same as any of our sensorysystems.Their pieces are united by our best guess of their function, based on the three types of convergingevidence discussedabove. Hence, we have concluded that the components of our visual systemtake the informationcontained in photons bouncing around in the world and use it to compute the location,orientation,texture,color, and movement of objects in the environment.The components of our auditorysys tem take the information contained in atmosphiericcompression waves and use it to compute the placementof things.And the components of our pain system take pressure, temperature,and chemical readingsof our surface (and interior) and use this information to track what is happening to our tissues.The A-8 cells and the C fibers do this, as do the spinothalamictractand its connections to the cortex.In sum, we have a complex but well-definedsensorysystemthat monitors our tissuesto promote the welfareof our bodies.37
35 Exactlywhat processing algorithmsare being executed is a more complicated stoxy, and one heavilyinfluenced by the pain inhibitoxysystem.Accounting for the details of the computationsis beyond the scope of this paper. 36 Critchley, aCongenital Indifference to Pain," Annals of Internal Medicine, XLV (1956):73747; R.A. Sternbach, aCongenitalInsensitivityto Pain:A Critique,"PsS chological Bulletin,LX ( 1963): 25244; and Pain: A Psychophysiological Analysis(New York: Academic, 1968). 37 See also Wall.This view, too, accounts for why our C-fibersystems might be so slow. General monitoring of bodily conditions should not often require a quick response.
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THEJOURNALOF PHILOSOPHY IV. STRANGE FACTSABOUT PAIN
As I stated in the introduction,the above is an easy and less interesting reason why philosophersare wrong. More to the point: this way of looking at our pain systemdoes not clear up all of the confusions, mysteries,and conflictsin our account of pain. There are severalimportantempiricalfactsthat any theoryof pain needs to be able to explain. These are facts that, by and large, do not have analogues in our other perceptualsystems.Moreover,they are facts that lead otheiwise intelligent people to make prima facie bizarrestatementsregarding what pain is and is not. Here, I can only touch upon a few such facts, but it should be enough to motivatethe challenge to theories of pain as well as to justify the approachI shall advocatein understandingpain phenomena towardthe end of this paper. (1) There is, in fact, a poor correlation between nociception and pain perception.38 That is, the relationshipbetween stimulatingthe A-8and C fibers and actuallyfeeling or reporting a pain is not at all straightforward. Several tribal rituals give vivid illustrationsof the dissociation. In parts of India, for example, men chosen to represent the gods have steel hooks inserted under the muscles of their back. They then swing above the crowds, suspended on these hooks by ropes, blessing children and crops. They exhibit no pain.39 I mentioned that about 40% of all emergency-roompatients reported feeling no pain at the time of injury;40% more report greater pain than one would expect, leaving only 20% of all emergency-roomvisitorshaving pains appropriateto their injuries.40 It is not the case that we can dissociatenociception from discriminative and affective-motivational reaction;it is that they regularlyand frequently dissociate. Our other perceptual systemsare not like this. There is a highly reliable correlationbetween havingthe rods and cones in our retina being bombardedby light photons and our havingsome visualexperience or other.41 There is also a highly reliable correlationbetween
38 Wall, She Dorsal Horn," in Wall and Melzack,eds., pp. 102-11;Wall and S.B. McMahon, aMicroneuronography and Its Relation to Perceived Sensation,"Pain, XXI (1985): 209-29. 39 D.D. Kosambi, aLivingPrehistory in India," Scientific Amerecan, cxan (1967): 105-14. 40 See Melzacket alia. 41 It is a live debate whether there is a good correspondence between the pattern of activityin the retina and a particulartypeof experience. How you answer that question depends upon how elastic you believe our visual amodule"to be. P*M. Churchland and R.L. Gregoxy,for example, think that our visual systemis cognitivelypenetrable from above;J. Fodor does not.
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the vibrationof our tympanicmembranesat a certain frequencyand hearing sounds. Any theoxyof pain is going to have to explain why our peripheralsensors for noxious stimuli do not appear to be wellconnected to our sensationsof pain. Indeed, relation between external events and internal indicators is part of what individuatesour systems.Without better correlation between an external event and internalactivity,we cannot claim that our putativepain systemis, in fact, a pain system. (2) Chronic pains are, by and large, a mystery.42 Some people have pains which last for years, with no discernible cause, and which are completely resistant to treatment. These are cases above and beyond things like phantom pains (which also have no discerniblecause and are resistantto treatment), for one might argue that phantom pains are simply abnormal instances of human su fering. (Who knows what is supposed to happen if you lose something as large as a limb? Surely, many areas of the topographically arrangedsomatosensory system will be thrown off track; maybe painsthat appear to be in the limb that no longer exists are not so strange after all.43) But with chronic pains, otherwise perfectly normalpeople-with no serious (or even superficial) injury - live their livesin constant pain. Moreover, removing bits of the spinal column,the dorsal horn, the thalamus, the reticular formation, the somatosensorycortex, or the frontal lobe concerned with pain have no effect on the patients being in pain. Again, there are few parallels with other perceptual systems. Rarely do otherwisenormal individualshave ongoing visualor auditoxy experiences without some determinate cause and explanaiion. Chronic hallucinaiionsby themselvesare quite rare. (3) Low-levelsiimulation of our thermoreceptors(the larger A-p fibers), which are not supposed to be connected to pain percepiion, inhibits the experience of pain,44 while a higher level siimulus exac42 KL. Casey, S. Minoshima, R.A. Koeppe, J. Weeder, and TJ.
Morrow, poro-Spatial Dynamicsof Human ForebrainActivityDuring Noxious Heat TemStimulation," Society of Neuroscience Abstracts, xx (1994): 1573; C.A. Due to Spinal Cord and Brian Stem Damage,"in Wall and Pagni, Central Pain Melzack,eds., pp. 634 43 Some phantom pains may be attributableto memories of recent amputated limb, for phantom pains bear an uncanny resemblance to pains in the pre-amputation experiences of pain. See J. Katz, Psychophysiological Contributionsto Phantom Limbs,"CanadianJournal of Psychiatry, xxxvrl (1992): EJ. Krane and L.B. Heller, zThe Prevalence of Phantom Sensation and 282-98; Pain in Pediatric Amputees," Journalof Pain Symptom Management, x (1995):21-29; Melzack, Phantom Limbs, the Self, and the Brain,"CanadianPsychology, xxx (1989): 44 Wall, Presynaptic Control of Impulses at the FirstCentral 1-16. Synapsein the Cutaneous Pathway," Physiology of SpinalNeurons: Progress in Brain Research XII (New
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erbatespain.45 Here, there are some parallelswith our other systems, if we take the A-,6interference to be a type of hard-wired pain illusion. Similarly, we see a straightstickas bent when placed half wayin water,and we arrangegroupsof dots into rowsand columns. Factssuch as these led the InternationalAssociationfor the Study of Pain (IASP)Subcommitteeon Classification to conclude: zPainis alwayssubjective.... Manypeople report pain in the absence of tissue damageor any pathophysiological cause;usuallythis happensfor psychologicalreasons.There is usuallyno wayto distinguishtheir experience from that due to tissuedamageif we take the subjective report... [P]ain...isalways a psychologicalstate)."46 Could they be correct?Are the connections between actual tissue damage, or some other injury, and our sensation of pain so weak that it is better to discount nociception entirelywhen defining pain?The IASPsubcommitteeclearly thinksso in their definitionof pain: ganunpleasantsensoryand emotional experience associatedwith actualor potentialtissuedamage,or described in termsof such damage" (ibad.; italicsadded). This sort of position is not preferable, for a variety of reasons. First,if pains are not correlatedwith actual injury,or the potential for damage, then we lose our intuitiveevolutionarystory about why we have a pain-sensingsystem.If our pain system has somehow become detached from the job it is supposed to perform,then its existence and poor performanceno longer have clear explanations. Second, pains become verypeculiarphenomena indeed, quite unlike our other qualitative experiences.We can havevisualor auditory hallucinations-we can be mistakenabout whatwe think we are perceiving-but if pain is purely subjective,then there is no way for us to have an illusion of being in pain. Phantom pains become just regular pains instead of some special case demanding special consideration and treatrnent.Of course, saying something is strange is not a reason for sayingthat it does not exist, but it is a reason, I believe, to be cauiious in makingsuch metaphysical commitments.Indeed, I do
York:Elsevier, 1964), pp. 92-118;Wall and Cronly-Dillon,Pain, Itch, and Vibration," Archives of Neurology, II (1960): 36S75; Wall and W.H. Sweet, Semporaly Abolition of Pain in Man,"Science, CLV (1967): 10849; see also W.D. Wlllisand R.E. Coggeshall, SensorR Mechanisms in theSpznalCord(New York:Plenum, 1978); T.L. Yakshe,Sptnal Af7rerent Processing (New York:Plenum, 1986). 45J.C.Wlller, F. Boureau, and D. Albe-Fessard,Human Nociceptive Reactions: Effects of Spatial Summation of Afferent Input from RelativelyLarge Diameter Fibers," BrainResearch, CI (1980): 46i70. 46InternationalAssociationfor the Studyof Pain (IASP) Subcommitteeon Classification, aPainTenns: A CurrentListwith Definitions and Notes on Usage,"Pain, Supplement 3 (1986), p. 217.
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think that the IASP subcommittee (and Colin McGinn and Saul are quite wrongin their understandingof whatpain is. Kripke)
OFPAIN THEORIES V. GATE
In general, gate theories of pain argue that the robust feedback loops in our pain systemserve to inhibit, enhance, or distortincoming nociceptive information.So, in addition to the basic six-neuron structureof our pain systemI outlined above, there are additional ascendingconnections from the spinal cord to the brain stem, circufrom the spinal cord to other areasin the spinalcord itlarpathways self, and descending feedbackloops from the cortex, hypothalamus, Some portions of this theand brain stem back to the spinal cord.47 oryhave been workedout in considerabledetail. Some of the mysterious pain phenomena can be explained in terms of well-confirmed gate theoryof pain. portionsof Melzackand Wall's48 Take the example of alteringour sensation of pain by stimulating the largerA-,6fibers.The AX and C neurons in the dorsal horn are connected via inhibitoryinterneurons.These interneuronsare stimulated by low-thresholdA-,6fibers. This means that stimulatingA-,6 cells dampens the activityof the Ak and C neurons in the dorsal horn, which in turn means that less pain informationwould travel (See figure 3.) Or, another example: gently pressup to the brain.49 ing a grid with alternating cool and warm bars on the skin often Neurophysiological causes the sensation of a strong burning pain.50 recordingsnow show that there are several ascending neurons that are sensitiveto both pain and temperature.A bit of centraldisinhibition plus these bimodal neurons explain how this illusion can occur. It can also explain why cold things burn.5lThe relaiionshipbetween taciile stimulaiion and pain is not completely clear here, however. Recent evidence indicates that painful stimuli can substaniiallydecreaseour sensationsof touch.52
See also Apkarian. 47 and TheChallenge Melzackand Wall, zPainMechanisms," Wall, Yntroduction"; 48
of Pain (New York:Penguin, 1986); see also N.F. Britton and S.M. Skevington,A Biolof Theoretical MathematicalModel of the Gate ControlTheoly of Pain,"Journal 0s2, CXXXVII(1980): 91-105. Severalaspects of the original theoxy have been shown Theoly: A Critto be incorrect;for discussion,see P.W.Nathan, The Gate-Control Brain,XCIX (1976): 12S58; and Kandeland Schwartz.Most accept the ical Review," general outline of the view, however. 49Wall, Introduction." 50 Known as Thunberg's thermal grill illusion, this was Elrstdemonstrated in 1896. 51A.D. Craig and M.C. Bushnell, The Thermal Grill Illusion: Unmasking the (1994): 252-55. CCLXV Burn of Cold Pain,"Science, R.A.Stea, and SJ. Bolanowski,Heat-Induced Pain DiminishesVibro52Apkarian, XI (1994): 25947. MotorResearch, tactilePerception,A Touch Gate,"Somatosensory
400
A-a andC hbers
1-1
1<
A-B hbers
10l
Figure 3. Low-levelgate control. Cells in the dorsal horn and trigeminal nuclei which respond to A-a- and C-fiber input have excitatory (filled circle) and inhibitory (open circle) interneuronsassociatedwith them. A-,lS fibers activatethe inhibitory neurons as well as input to the nociceptive cells. Descending controls input to the interneurons.
Moreover, though more research needs to be done, the alternate routes in the central nervous system might help explain why cutting the primary dorsal horn pain channel, or parts of the spinal cord itself, may not remove chronic pain.53 Indeed, it looks as though the failure at curing chronic pains by lesions is overstated anyway.54 Some neuropathic pains are controllable using subarachnoid opioids, as they interfere with the pain centers in the dorsal horn, which are probably responsible for deafferantation pain.55Other data indicate that most chronic or prolonged pains are the result of changes in central nervous functions that have been caused by the neural firing patterns of early nocicew
tion.56
A Melzack-Wall type of gate-controltheory of pain cannot be the entire story, however, for three reasons. First,we do not have anything approachinga complete theory at this stage in the game. A153 S. Canavero,Dynamic Reverberation: A Uniled Mechanismfor CentS and Phantom Pain,"Medical Hypotheses,XVII (1994): 203 07; see also A. Dray,L. Urban, and A. Dickenson, Pharmacology of Chronic Pain," Trends in Phar7nacological Sczence, xv (1994): 190-97. 54 See Canavero. 55 R.P. Iacono, M.V. Boswell, and M. Neumann, Deafferentation Pain Exacerbated by SubarachnoidLidocaine and Relieved by SubarachnoidMorphine:Case Report,"Regional Anesthesiology (United States),xz (1994): 212-15. 56 See discussion and review in A.L. Vaccarino and D.A. Chorney, Descending Modulation of CentralNeural Plasticityin the FormalinPain Test,"Brain Research, DCIXVI ( 1994): 104-08.
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though the theory does explain low-levelphenomena, nothing has been worked out in particularregardingthe clearly apsychological" influences.57 Melzackand Wall themselves simply gesture towarda central gating mechanism that presumablywould explain hypnosis effects, any remaining chronic pains, the dismal correlations between emergency-room injuriesor back injuriesand pain, and so on. But without providing more details where this central gating mechanismis located in the brain, how it functions to alterour pain perceptions, why we have such a powerful mechanism, for example then they have said little more than that "someother stuff happens in the head that explains everything else." As Wall himself remarksof the manyareasimplicatedin inhibiting our sensationsof pain: aunfortunately we know little of their relativeimportanceand nothing of the actual circumstances in which they come into
action."58
Second, and more importantly, even if we could get the detailson some sort of central gating mechanism, this would not mean that pains are not largelysubjective(which is but a step awayfrom being purely subjective). If top-down cortical processes (which is what I take 'purelysubjective'to mean here) are mainlyresponsiblefor our sensationsof pain, then the IASPsubcommitteewould be right and pains would be deeply peculiar.They would be the only perceptual experiences we have which are normal (that is, normal functioning creatureshave them), natural (that is, not the product of tweaking something in a laboratory,but occurring in the wild, as it were), commonplace (we have them all the time), believed to be giving us informationabout the external environment (external to the brain, that is (but internal to our bodies)), but in fact not. Dreamsmight be the only exception, but, unlike dreams,we do not realizewhen a pain is over that it reallywasnot about the externalworldafterall. Finally,athe body of psychologicalresearchinto pain has failed to yield compelling evidence for a direct causal relationship between psychologicalfactorsand pain in the general population of pain patients."59 In general, if physicianscannot find a physicalcause for a pain and it continues despite medical interventions,then it is attriS 57 The influence of the psychologicalon the perception of pain has a long and venerable history;see Whytt (1786), Brodie (1837), Carter (1853), as described in H. Merskeyand F.G. Spear, Pain: Psychologicaland Psychiatrzc Aspects (London: Balliere, Tindall, and Cassell,1967). 58Wall, aIntroduction," p. 12. 59 A. Gamsa, aThe Role of PsychologicalFactors in Chronic Pain, II: A Critical Appraisal," Pain, LVII ( 1994): 23.
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uted to something "psychological" (ibid.).60 This can be at best an unsupported hypothesis,however.At worst,it is a euphemism for our own ignorance. If pains are driven by psychologicalfactors,then we should be able to isolate what those factors are. Thus far, we have been unsuccessfulin discoveringany psychologicaltrait or ailment that is correlated with sensations of pain. In sum: those who claim that pain is subjectiveor psychologicalare being too facile. Mostphilosophers, psychologists, and neurophysiologists who do not fall preyto the less interestingmistakedo hold some versionof a gatecontrol theory. Some advocate it explicitly (for example, Dennett, Melzack, Wall);othersmaintainit implicitly (Hilgard,Tye). Eitherway, I believe this commitmentto be premature. If there is any wayfor us not to hold that our pain systemis purely,or largely,or even significantlysubjective, then we should not do it. I proposethatinsteadof acquiescingto the IASPsubcommittee's conclusion,we should talQe the mysterious and unexplainedpain phenomenaas evidencethat the sixneuron view (even with the additionalbells and whistles)is wrong.I suggestthatwe shouldreexarnine the datafFoma differentperspective.
VI. A PAIN-INHIB1TING SYSTEM
If standard (higher level) gate-theory approaches are misguided, then we still have a chance at understandingpain from a solid neurophysiologicaland biological perspectivewithout making pain into something peculiar.As will be clearin a moment, I advocatedividing what Melzacket alia have lumped into one corticallyclrivenpain system into two separate systems:a nociceptorZrivenpain sensorysystem (PSS) and a largelytop-downpain inhibitorysystem(PIS). First, though, let me sketch some data that I believe are relevant to this perspective,data that the more traditionalgate theories either overlook or minimize; I shall then outline some theoretical considerations that point towarda two-system model. Proponentsof gate theorieswriteas thoughjust about any psychological event or any area of the cortex has the potential of influenc60R.C. Kupers,H. Konings, H. Andriaensen,and J. Gybels,EIorphine DifferentiallyAffects the Sensory and AffectivePain Rating in Neurogenic and Idiopathic Forms of Pain," Pain, XLVII (1991): 5-12; see also discussion in S. Benjamin, D. Barnes, S. Berger, I. Clarke, and J. Jeacock, Yhe Relationship of Chronic Pain, Mental Illness, and Organic Disorders,"Pain, xxxrs (1988): 185-91;M. Grushka, BJ. Sessle, and R. Miller, aPain and PersonalityProfiles in Burning Mouth Syndrome,"Pain, XXVIII(1987): 15S67; H. Merskey,aSymptoms that Depress the Doctor, Too Much Pain,"BrztishJournal ofHospitalMedicine (January 1984): 6S66, and aPsychiatlyand Chronic Pain," Canadian Journalof Psychiatry, XXXIV (1989): 32935; R.A. Sherman, CJ. Sherman, and G.M. Bruno, aPsychologicalFactors Influencing Chronic Phantom Limb Pain: An Analysisof the Literature,"Pain, xxvm (1987): 28S95.
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ing the perception of pain, what Melzack calls a neuromatrzx.61 A1though there are lots of feedbackloops and other sorts of pain connections, not everyarea in the brain is sensitiveto pain information. Recent advancesin functional imaging technology which includes magnetic resonance imaging (MRI),xenon gamma emission detection, single photon computer emission tomography (SPECT),and positron emission tomography(PET) allow us to map active areas of the brain with greater precision than ever before.62 Imaging studies of pains clearly show that chronic pains are correlated with increased activity in the cingulate and frontal cortex, as well as sometimeswith the insular cortex, hypothalamus,and periaqueductal gray.63 Phasic pains are keyed to increased activityin the anterior cingulate, frontal cortex, thalamus,and primaryand secondarys matosensorycortex.64 Although lack of activitydoes not prove con61 Melzack, aPhantomLimbs and the Concept of a Neuromatrix,"Trands in Neurosciance, xm(1990):88-92;"Central Pain Syndromesand Theories of Pain,"in E.L. Casey,ed., Pain and Cantral Nersous Disease: The Central Pain Syndrtzmes (New York: Raven, 1991), pp. 59-64, and aPhantomLimbs,"ScientificAmencan, CCLXVI (1992): 9S96; see also discussionin Canavero. 2 See Apkarian. 63 y. Hosobuchi, aTreatment of CerebralIschemiawith ElectricalStimulationof the CervicalSpinal Cord,"Pace,XIV (1991): 122-26;Y. Katayama, T. Tsubokawa, T. Hirayama,G. Kido, T. Tsukiyama,and M. Iio, aResponse of Regional Cerebral Blood Flow and Oxygen Metabolism to Thalamic Stimulation in Humans as Revealed by Positron EmissionTomography,"Jour7zal of Cerebral Blood FlowMetabolzsm, VI (1986): 63741; E.C. La Terre, A.G. De Volder, and A.M. Goffinet, aBrainGlucose Metabolismin Thalamic Syndrome," Journalof Neurosurgery and Psychiatry, LI (1988): 427-28;Y.R.Tran Dinh, C. Thurel, A. Serrie, G. Cunin, andJ. Seylaz,gGIycerol Injection into the Trigeminal Ganglion Provokesa Selective Increase in Human CerebralBlood Flow,"Pain, XLVI (1991): 1S16. 64 Apkarian;Apkarian,R.A. Stea, S.H. Manglos,N.M. Szeverenyi,R.B. King, and F.D. Thomas, gPersistentPain Inhibits Contralateral SomatosensoIyCorticalActivity in Humans,"Neuroscience L^etters, CXL (1992): 14147; M. Backonja,E.W. Howland, J. Wang,J. Smith, M. Salinsky,and C.S. Cleeland aTonic Changes in Alpha Power During Immersion of the Hand in Cold Water" Etectroencepholography and Cl?nical Neurophysiology, LXXIX (1991): 192-203;E.L. Casey,ed. Pain and Central NervousDisease; KL. Casey,S. Minoshima,KL. Berger, R.A.Koeppe, TJ. Morrow,and KS Frey, gPositronEmission Tomographic Analysisof Cerebral StructuresActivated Specifically by Repetitive Noxious Heat Stimuli,"Journalof Neurophysiologzy, LXXI (1994): 80247; R.C. Coghill, J.D. Talbot, A.C. Evans, E. Meyer, A. Gjedde, M.C.Bushnell, and G.H. Duncan, gDistributed Processingof Pain and Vibrationby the Human Brain,"Journal of Neuroscience, XIV (1994): 4095-108;V. Di Piero, S. Ferracuti,U. Sabatini,P. Pantano, G. Cruccu,and G.L. Lenzi, gACerebralBlood Flow Studyon Tonic Pain Activationin Man,"Pain, LVI (1994): 167-73;G.H. Duncan, C. Morin,R C. Coghill, A. Evans,KJ. Worsley,and M.C. Bushell, gUsingPsychophysical Ratingsto Map the Human BrainRegression of Regional CerebralBlood Flow (RCBF)to Tonic Pain Perception,"Soczety of NeuroscienceAbstracts, xx (1994):1572; J. Hsie, O. Hagermark, M. Stahle-Backdahl, K Ericson, L. Eriksson, S. StoneElander, and M. Ingvar, gUrge to Scratch Represented in the Human Cerebral Cortex During Itch,"Jour7lal of Neurophysiology, LXXII (1994): 3004-08;SKP. Jones,
404
clusivelythat an area is not sensitiveto pain information,these sorts of studies should give advocatesof global corticalinfluences on our perceptionof pain pause for thought. Moreover, the neuronal areas sensitive to pain information are different from what we originallybelieved. Rat studies suggest that, in addition to the structures discussed above, areas of the limbic systemare also involved.65 Functional images of human brains indicate that homologous areas are involved in us as well.66 Moreover, limbic activityin chronic pains becomes quite important as imaging studies also show a decrease in thalamic activity,instead of the increase one would expect. The decrease in thalamic activity,coupled with the increase in cingulate response, tells us that a spinothalamicpathwaycannot be what is causing the increase. Scientists have discovereda direct connection between the spinal-cord projectionsand multiple limbic areas in both the rat and monkey.67 The limbic systemis then tightly connected with the cingulate and frontal cortex. The limbic system also receives inputs from the reticularsystem (another painjuncture). As Apkarianconcludes, Zthebrain imagining studies of pain...point to a very different emphasis in research regardingthe central processing of pain.... [S]ystemsoutside of the spinothalamic system may control the type of processing taking place in the spinothalamic system. [Chronic pains]...seem to ac6vate cortical areas outside the spinothalamicdomain, which in turn inhibit the spinothalamic inputs to the cortex" (op. cit., p. 290). That the thalamus and cortex are probablynot important in processing our perceptions of pain stands in direct contrast to what many take to be common knowledge regarding how our pain system works. Because new facts regardingthe transmission of pain information in the brain are only slowlyemerging, we should be fairlyconservative in our conclusions.All I want to claim at the moment is that the
W.D . Brown , KJ. Friston , L.Y. Qi , and R.SJ. Frackowiak, gCortical and Subcortical Localization of Response to Pain in Man Using Positron Emission Tomography," Proceedings of the RByalSociePy of London, CCXI1V (1991): 39a;J.D. Talbot, S. Marrett, A.C. Evans, E. Meyer, M.C. Bushnell, and G.H. Duncan, gMultiple Representations of Pain in Human Cerebral Cortex," Science,CCLI (1991): 135S58. 65J. Mao, DJ. Mayer, and D.D. Price, aiPatternsof Increased Brain Activity Indicative of Pain in a Rat Model of Peripheral Mononeuropathy,"Jou7nal of Neurosczence, XItI(1993): 2689-702. 66See Apkarian; and Roland. 67Apkarian; H.M. Newman, R.T. Stevens, C.M. Pover, A.V. Apkarian, gSpinalSuprathalamic Projections fFom the Upper Cervical and the Cervical Enlargement in Rat and Squirrel Monkey," Socielvy of NeurosczenceAbstracts, xx (1994):118.
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six-neuron sketchof nociceptiontransmission is probably oversimplifiedto the point of being misleading. Acceptingthis conclusion opens the possibility of describing our painsystems differently than it has been in the past.Moreimportant for our purposes, it allows the possibility of dividing whatwe havebeen callingour painsystem into twodifferent andindependent processing streams. I shallargue thatdoingso helpsclearup the remaining puzzles in painphenomena. We have known for some time that many of the inhibitory streamsare not merely feedback loops in our ascending pain Elbers, for theyare anatomically distinctfromour pain processors. Threeareasare primarily responsible for inhibitingpain information in the spinalcolumn:the cortex,the thalamus, and the brain stem. The dorsalraphe is probablyheavilyinvolvedas well.68 In particular, the neocortexand hypothalamus projectto the periaquaductal grayregion (PAG),which then sends projectionsto the reticularformation(see figure 4). The reticularnuclei then workto inhibitactivity in the dorsalhorn.69 Thisprocessing stream worksby preventing a centralcorticalrepresentation of painfrom forming.70 Endogenousopioids, stimulatingthe PAG,and morphine all dampenincominginformationin the same wayin the dorsalhorn. That is, this pain inhibitionstreamdoes not merely disruptthe transmission of pain information, it actively prevents it fromoccurring. In addition, thissubsystem is not the onlypain inhibitor at work. Stress-induced analgesiacan occur withoutany opioidsbeing releasedand it is not prevented fromoccurring whenopioid-blockers areadministered.71 Moreover, different neuralsubstrates areinvolved in inhibiiing fastpainsandslowpains.Stimulating the hypothalamus reduces tonicpainandis not related to stress-related analgesia.72
68tp. Wang and Y. Nakai, She Dorsal Raphe: An ImportantNucleus in Pain Modulation," BrainResearch BuUetin, VI (1994): 575. 69H.L. Fields, gAn Endorphin-MediatedAnalgesia System, Experimental and Clinical Observations," in J.B. Martin,S. Reichlin, and KL. Brick, eds., Neurosecro tion and BrainPeptides, Implications for Bnan Functionand Neurological Disease(New York:Raven, 1981); H.L. Fields and A.I. Basbaum, gEndogenous Pain Control Mechanisms," in Wall and Melzack,eds., pp. 20S19; for references and reivew,see alsoJ.E. Sherman and J.C. Liebeskind, gAnEndorphinergic,CentrifugalSubstrate of Pain Modulation:Recent Findings, CurrentConcepts, and Complexities," inJJ. Bonica, ed., Pain (New York: Raven, 1980), pp. 191-204. 70 See Vaccarinoand Chorney. 71 See Kandeland Schwartz; and Fields and Busbaum. 72 R. Lopez, S.L. Young,and V.C. Cox, Analgesia for Formalin-Induced Pain by LateralHyr pothalarnicStimulation," BrainResearch, DLXIII( 199l ): 1-7.
406
OF PHILOSOPHY THEJOURNAL | Fronta Cortex
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atosensory
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in contrast to the pain Figure 4. Diagram depicting the pain inhibitory system hypothalamus descend and cortex the in sensory system. Projections originating formation, and then fito the periaqueductal gray of the midbrain, the reticular nociceptive transmisascending the inhibit they where horn, dorsal the nally to sions.
dissociaMore important than being anatomically distinct and disteleologically are streams ble from nociception, the inhibitory not are streams inhibitory The tinct from our PSS system as well. very a by triggered are they merely general purpose dampers; Otherspecific constellation of peripheral and cortical inputs. of sensations our increase wise, their removal would drastically Lethough. case the not is pain or make them all chronic. Such onset of sioning the PAG does not appear to be tied to the
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chronic pains.73Moreover, we do know that the inhibitory systems are activated (or inhibited) by nociception plus cortical arousal (stress) on the organism.74 Fear and learned hopelessness also affect their activity.75 Hence, the correlates for the Elringof these neurons differ in kind from what our ascending pain system is sensitive to. In addition, if we look at the connections of the inhibitory streams, we can see that they differ substantiallyfrom the PSS. It would not be proper to call them sensorysystemsor subsystemsfor they have no connections to the periphery. The pain inhibitory streams halt at the dorsal horn. Also unlike our ascending pain streams,the hypothamalusand dorsal raphe nuclei receive massive inputs from cortical processors,which presumablycould carryinformation about our goals and immediate plans, what else is occurring in the environment, and our emotional context.76 They have immediate access to information that the ascending pathwaysdo not. Finally,a two-systemtheory of pain sensation explains our evolutionary confusions. When we are under stress, it is often more adaptive not to feel pain than to be incapacitated by pain.77 If we are Elghtingor fleeing from an enemy, it would be preferable to do so unencumbered by the need to nurse or protect our limbs, even if this results in more nursing or protecting later (when we are presumablysafe). It is important to know when damage is occurring in our bodies, but it is equally important to be able to shut that information out when circumstances demand. A dual system 73 See Pagni. 74 Fieldsand Basbaum; M.L.Mayer,aPeriaqueductal GrayNeuronal Activity, Correlation with EEGArousalEvokedby Noxious Stimuli in the Rat,"Neuroscience Letters, xxvm (1982): 297-301. 75 S.F. Maier, R.C. Drugan, J.W. Grau, "Controllability, Coping Behavior, and Stress-inducedAnalgesia in the Rat,"Pain, XII (1982): 47-56;J.W. Lewis,J.T. Cannon, andJ.C. Leibeskind, "Opioidand Non-opioid Synapse Mediates the Interaction of Spinal and Brain Stem Sites in Morphine Analgesia," Brain Research, CCXXXVI (1980): 8S91;J.W. Lewis,J.E. Sherman,and J.C. Leibeskind, "Opioidand Non-opioid Stress Analgesia, Assessment of Tolerance and Cross Tolerance with Morphine," Journalof Neuroscience, I (1981): 35843; J.W. Lewis, M.G. Tordoff,J.E. Sherman, and J.C. Liebeskind, "AdrenalMedullaxyEnkephalin-likePeptides May Mediate Opioid Stress Analgesia,"Science, CCXVII (1982): 557-59; Fields and Basbaum. 76 See Kandeland Schwartz. 77 RJ. Bodnar, "Effects of Opioid Peptides on Peripheral Stimulation and 'Stress'-Induced Analgesiain Animals,"Crxtical Retnezvs in Neurobiologzy, VI (1990): 3949; Kandel and Schwartz; J.I. Szekely,"OpioidPeptides and Stress,"Critical Reviezvs inNeurobiologzy,vi (1990): 1-12.
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would allowjust such a contingency; we could inhibit our pains as needed, but then feel them again when the danger is gone. A PSS and a PIS then serve two different goals: the PSS keeps us informed regarding the status of our bodies. It monitors our tissues to maintain their intactness whenever possible. In contrast, the PIS shuts down the PSS when flight or fleeing is immanent, and then enhances the PSS response in moments of calm. If our brains are geared for motor control, then the dual pain system makes good biological sense. In sum: the bottom-up and the towdown investigativestrategies support the conclusion that our pain inhibitorsform a separateand distinct system. They react to different types of stimuli. They have different points of input and output from the PSS, and their existence is supportedby evolutionary considerations.
VII. REPRIEVE: THE SENSATION OF PAIN
If my story is correct, then, contraryto how things seem to us, the sensation of pain is not what is most important in pain processing. It is but one minor aspect of our entire pain and pain-inhibitory systems, which themselves are geared to help us flee, fight, or nurse ourselves, depending upon the circumstances. They function just as any of our perceptual systems do: they help us get around in our environment as effectively as possible. From an evo lutionary perspective, visual sensations are not the raison d'e^tre of our visual system, and auditory sensations are not the ultimate goal for our auditory system. Sensations of pain are no different. Insofar as the PSS is simpler than other perceptual systems,then it makes good sense to use pain as a paradigm case of our conscious
experiences.
We must issue an importantcaveat,however:pains are the product of a complex sensory system that has to struggle to get itself heard. Our conscioussensationsare the productof both nociception and activityof a PIS.78 Even though nothing about painful experiences is deeply mysterious-they are not random, nor inexplicable, nor tied to our psychologicalwhim& they still are poorly correlated with actual tissue damage. What is interesting and different about our pains is the PIS. It is geared to suppressor enhance the activity of a single sensorysystem,and there is no other systemquite like it in our nelvous system.We do have general inhibitoxyand excitatory
78 This iS not to say that the PIS is directlyconnected to our sensations of pain. It is not. We can remove bits and pieces of the PAG,for exarnple,and still feel pain. Nevertheless,the PIS heavilyinfluences when and where we feel pain.
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systemsin the brain, but none of these is specific to a particularsensorysystem.The PISentails that our sensationsof pain are almostindependent of nociception. Hence, insofaras we have a PIS,then our sensationsof pain are special and are not a typicalexample of a phenomenological process. Putnam and others are simply wrong to think of a pain as the exemplarof consciousness.
VALERIE GRAYHARDCASTLE
Mlrginia PolytechnicInstituteand State University

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Journal of Philosophy, Inc.

THE JOURNAL OF PHILOSOPHY VOLUMEXCIV, NO. 8, AUGUST 1997

Eliminativist Completely Objective

Relation Purely subjective |

Conee Nelldn Kaufman

I. THE COMPLEXITY OF OUR SENSORY SYSTEMS

the thalamusin Pain:

A Spzk0Interoal(ided Messagein theBrain (NewYork:Raven, 1981).

WHEN PAINIS NOT

Part of the Body

THEJOURNALOF PHILOSOPHY IV. STRANGE FACTSABOUT PAIN

WHEN PAIN IS NOT

PAINIS NOT WHEN

A-a andC hbers

WHEN PAINIS NOT

OF PHILOSOPHY THEJOURNAL | Fronta Cortex

Co rt ical ject io ns Pro

Periaqueducte Gray Region

Mlrginia PolytechnicInstituteand State University

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