Mind-brain correlations, identity, and neuroscience

17 Pages·00.09 MB·English

by  Brandon N. Towl

PhilosophicalPsychology
Vol.25,No.2,April2012,187–202
Mind-brain correlations, identity, and
neuroscience
Brandon N. Towl
One of the positive arguments for the type-identity theory of mental states is an
inference-to-the-best-explanation (IBE) argument, which purports to show that type-
identity theory is likely true since it is the best explanation for the correlations between
mentalstatesandbrainstatesthatwefindintheneurosciences.Butgiventhemethodsof
neuroscience,thereareotherrelationsbesidesidentitythatcanexplainsuchcorrelations.
I illustrate some of these relations by examining the literature on the function of the
hypothalamusanditscorrelationwithsensationsofthirst.Giventhattherearerelations
besidesidentitythatcanexplainsuchcorrelations,thetype-identitytheoristisleftwitha
dilemma: either the correlations we consider are weak, in which case we do not have an
IBE to an identity claim, or else the correlations we look at are maximally strong, in
which case there are too few cases for the inductive part of the strategy to work.
Keywords: Hypothalamus; Identity Theory; Inference to the Best Explanation; Kind
Splitting; Mind-Brain Correlations; Psycho-Physical Correlations; Thirst
1. Introduction
The identity theory, the theory that mental states are type-identical to brain states,
hasbecome popularagain (for examples, seeKim, 1993,1998; Mandik, unpublished
manuscript; Polger, 2005; Shapiro, 2004). Though many authors have written
defensesofthetheory,thepositiveargumentsforidentitytheoryhavenotreceivedas
much scrutiny. Here I would like to examine the argument that starts with (what
some call) the psycho-physical correlation (PPC) thesis. The argument tries to
establishthatthePPCthesisprovidesgoodevidencefortype-identitytheorybecause
type-identitygivesusthebestexplanationofwhythePPCthesisholds.Thuswehave
an inference-to-the-best-explanation (IBE) argument for the type-identity theory,
given the PPC thesis. This strategy can be found explicitly in the earlier works of
Christopher Hill (1991, 1984) as well as more recent work by Brian McLaughlin
(1997, 2001; Hill & McLaughlin, 1999).1
BrandonN.TowlisalectureratWashingtonUniversityinSt.Louis.
Correspondenceto:BrandonN.Towl,WashingtonUniversity,St.Louis,MO,USA.Email:[email protected]
ISSN0951-5089(print)/ISSN1465-394X(online)/12/020187-16(cid:2)2012Taylor&Francis
http://dx.doi.org/10.1080/09515089.2011.569920
188 B. N. Towl
Aftersettingouttheargument, Ishallarguethatitfacesadilemma thaterodesits
initial appeal as justification for type-identity theories. Specifically, correlations
betweenmentalstatesandbrainstatesareeitherrelativelyweakorstrong.Ontheone
hand,weakcorrelationscouldbeexplainedbyidentifyingamentalstatewithabrain
state—but there are a number of other relations that can explain such correlations
as well. On the other hand, if the identity theory is meant to explain only strong
correlations, it turns out that there are very few of these—too few to justify the
induction thatallmental states,as wecurrently describethem,areinfact brainstates.
2. The Psycho-Physical Correlation Thesis and IBE
The psycho-physical correlation thesis is usually stated thus:
Psycho-physicalcorrelationthesis(PPC):foreverytypeofmentalstate,M,thereis
atypeofphysical(orfunctional)stateP,suchthatitisnomicallynecessarythatfor
any being x, x is in M if and only if x is in P.2,3
ForthePPCthesistoserveasapremiseinanIBEargumentforanidentitytheory,
it must represent a summary of empirical findings thus far. The PPC thesis is more
happily read, then, as a summary of certain observations made in the course of
neuroscience. Such correlations populate the neuroscience literature: fear is
correlated with activity in the amygdala, pain is correlated with activity in the
somatosensory cortex, visual sensations are correlated with activity in V1, etc. This
means the PPC thesis is not to be read as the conclusion of an a priori metaphysical
argument.Rather,theideaisthatthetruthofthePPCthesisisestablishedbyfinding
a sufficient number of mind-brain correlations, while the explanation of the PPC
thesis,iftrue,isthatidentitiesholdbetweenthementalstatesandthephysicalstates
being referred to.
Manyauthorsdobelievethat(1)therearecorrelationsbetweenmentalstatetypes
and physical state types,4 and (2) that these correlations do provide evidence for
identity based on an IBEargument. Theargument takes roughly thefollowing form:
First Premise: if a theory provides a good explanation of a set of facts, and the
explanationisbetterthananyexplanationprovidedbyacompetingtheory,then
one has a good and sufficient reason to believe that the theory is true.
(IBE Principle)
Second Premise: type materialism [a.k.a., type identity theory] provides a good
explanationofthepsycho-physicalcorrelationsthatareclaimedtoexistbythe
PPC.
Third Premise: moreover, the explanation that it provides is superior to the
explanations provided by all competing theories.
Conclusion: provided that the psycho-physical correlation thesis is true, we have
goodandsufficientreasontobelievethattypematerialismistrue.(Hill,1991,p.
23)
Hill’sargumenthereisaclearstatementofthestrategy,andsomakesagoodtarget
for the ensuing discussion. Indeed, on its face, this argument seems sound (it is
Philosophical Psychology 189
certainlyvalid).Aproblemarises,however,dependingonwhatwetakeourevidence
for the second premise to be.
Consider: the PPC thesis, as stated, implies that the correlations to be found
betweenmentalstatetypesandbrainstatetypeswillberelativelystrong,meaningthat
there will be few to no exceptions. It also implies that there will be a strong
correlation for every mental state type of interest. (More will be said about
correlations andtheirrelativestrengthbelow.)Thesetwoimplicationsareintension
with each other: if the correlations to be explained are strong, then they are unlikely
to apply to all cases of mental states of interest. Likewise, if we wish to capture all
mental states of interest, the correlations we wish to explain might be relatively
weak—and then the identity theory is a less viable explanation for them (or so I
shall argue).
Put another way: if the identity theorist seeks to explain (relatively) weak
correlations, thenthethirdpremiseisfalseand theIBE argument fails. Ontheother
hand,if onlymaximally strong correlations are allowed, thenthePPCthesis willnot
hold true for many pairings of mental states and physical states that are of interest,
and the identity theory loses its generality as a theory of mind.
Inthenextsection,Ioutlinethewaysthatmind-brain correlations areestablished
empirically to provide background for the discussion to come. In sections 4 and 5,
I will look at the first horn of the dilemma, that identity might not be the best
explanation for weak correlations. Section 6 will look at the other horn: focusing on
maximally strong correlations erodes the appeal of an identity theory as a general
theory of mind. I end with some common objections to my argument in section 7.
3. Mind-Brain Correlations
Tosaythat‘‘Mis(type)identicaltoB’’istomakeakindofmetaphysicalclaimabout
the kinds of things named by ‘M’ and ‘B’.5 A mind-brain correlation, on the other
hand,isapatternofco-occurrencebetweenagivenMandagivenB.ThePPCthesis
claims that there will be a mind-brain correlation for every mental state of interest,
while the IBE argument provides evidence for the identity theory based on these
correlations.
So what exactly does it mean to say that a mind-brain correlation is a ‘‘pattern of
co-occurrence between a given M and a given B’’? Roughly, when a type of mental
stateispresent,atypeofbrainstatealsoseemstobepresent(andviceversa).Amore
rigorousdefinitionofmind-braincorrelationcanbehadintermsofgoodevidencefor
the presence or absence of a given state:
Mind-brain correlation: a mental state type M is said to be correlated with brain
state type B iff, forall (ormost) tokens ofM and B, thefollowing criteria obtain:
(1) WhenwehavegoodevidencethatamentalstatetokenofMispresent,wealso
have (or could obtain) evidence that a brain state token of B is present
(M!B);
190 B. N. Towl
(2) When we have good evidence that a brain state token of B is present, we also
have (or could obtain) evidence that a mental state token of M is present
(B!M);
(3) When we have good evidence that M is absent, B also appears to be absent
((cid:2)M!(cid:2)B); and
(4) When we have good evidence that B is absent, M also appears to be absent
((cid:2)B!(cid:2)M).6
And so there are actually four kinds of evidence we can look for in order to
establish a mind-brain correlation. If we have all four kinds of evidence, and the
evidence is good, we can say that we have a strong correlation. If we have fewer than
these four, or if some of the evidence is contested, we can talk about a weaker
correlation.7 It should not be surprising, given the above, that the methods
neuroscientists employ to look for such correlations mirror these criteria.8 For
example, neuroscientists do experiments that:
(1) Activateagivenbrainstate,andthenmeasurewhetherornotagivenmentalstateoccurs.
Examples of such ‘‘activation’’ studies include direct stimulation experiments using
electrodes or chemical intervention, as well as indirect stimulation studies using
administered drugs;
(2) Prevent,destroy,orhandicapabrainstate,andmeasurewhetheragivenmentalstatesis
absent. Most lesion studies fall under this category, as do experiments that pharmaco-
logically block the activity of a mechanism and ‘‘knock out’’ studies that prevent the
expression ofgenes responsible for generating certain kinds ofstructures;
(3) Present stimuli constructed to activate a given mental state, and then look for
correspondingbrainstates.Mostimagingexperimentsfallunderthiscategory,asdoEEG
experiments; and
(4) Presentstimulithatpreventordeactivateamentalstate,andthenseewhichbrainstates
are absent. Though much more rare, such experiments do exist. For example, there are
fMRIexperimentsthatrevealdifferencesinbrainactivitywhenasubjectinanexperiment
hasfailedtoencodeapieceofinformation,asshownbysubsequentforgettinginarecall
task.
In other words, the various methods that neuroscientists actually employ mirror
the criteria from the definition above. If all four types of experiment are done for a
givenMandB,andtheseexperimentsshowthatMdoesinfactcorrelatewithB,then
we have a strong correlation between the two.
There could be many or few mind-brain correlations (a correlation is between a
given M and a given B, after all). And some mind-brain correlations might be weak
whileothersarestrong.ThisfactsuggeststhattheargumentgivenbyHillneedstobe
broken intotwosteps.First, ifamind-brain correlation isfound, thereisapotential
IBE argument for a single identity claim—that is, that a given M is type-identical to
agiven B.Second, there needs tobe aninductive argumentto establish amind-brain
identity theory that covers all (or most) mental states.9 The inductive argument is
needed for the identity theory to be a general theory of mind: finding a correlation
between one mental state and one brain state, though interesting, would not be
adequateevidencetobuildanargumentfortheidentitytheory,ageneraltheoryabout
Philosophical Psychology 191
mental states. After all, if we found that pain, say, correlated strongly with C-fiber
firing,butthatnoothermentalstateseemedtocorrelatewithanyknownbrainstate,
no one would claim that we have identity theory of mind (though we might have a
case for a single identity claim). It would have to be the case, then, that
neuroscientists findmanymind-brain correlations—enough to support aninductive
argument for identity theory.
Now we can bring the initial tension into better focus. As mentioned previously,
correlations can be weaker or stronger. If we allow weak correlations to provide
evidenceforthePPCthesis,thenitisunclearthatarelationofidentitywillalwaysbe
thebestexplanationforthosecorrelations.Ontheotherhand,ifweallowonlystrong
correlations to provide evidence for the PPC thesis, then there are vanishingly few
such correlations—so much so that the inductive step becomes suspect.
In summary, I am suggesting that it is misleading to ask whether type identity
theory is the best explanation for the PPC thesis (as stated). Rather, we need to ask:
(1) ‘‘for individual cases, would an identity claim be the best explanation for a given
mind-brain correlation?’’ and (2) ‘‘are there enough such identity claims to merit a
general identity theory?’’10
4. Identity Claims and Correlation
Let us examine the former question first—whether identity claims are a sufficient
explanation for a given mind-brain correlation. Kim (2005) has recently argued that
identities are not actually explanatory, and thus that IBE arguments for identity
theory will fail (thus denying Hill’s second and third premises). Briefly, Kim argues
that identity claims simply afford re-write rules that allow us to rephrase statements
about mental states into statements about neural states. Any actual explanation that
occurs, however, is done outside of the identity statement.
Kim seems to consider two types of correlation through his given examples:
correlations between phenomena that are diachronic, and correlations between
phenomena that are synchronic. Diachronic phenomena are perhaps best explained
intermsofcausalchains;theyarenotthesortsofcorrelationsbeingconsideredhere.
The sorts of correlations that Hill, McLaughlin, and others are concerned with are
synchronic—that is, where tokens of the types involved co-occur. So let us focus on
Kim’s synchronic example.
Kimprovidesonesuggestedderivationofacorrelationfromanidentitystatement:
Pain occurs$pain occurs.
Pain¼Cfs [C-fiber firings].
Therefore, pain occurs$Cfs occur. (Kim, 2005, p. 135)
In this example, the correlation is derived from the identity statement plus a
tautology. But, says Kim, the only explanatory premise is a factually empty logical
truth (the tautology); the identity claim here simply allows us to rewrite this truth
using substitution. This sort of explanation, for Kim, ‘‘is a far cry from genuine,
192 B. N. Towl
factually substantial and empirically falsifiable, explanations of correlations found in
science’’ (2005, p. 136).
Kim’s assessment is a bit unfair. First, even if identities only provide ‘‘re-write’’
rules, identities of the form ‘a¼b’ can still be informative. And if they are
informative, we should not pass them off as just rewrite rules. Second, and more
importantly, identitiescanhaveexplanatorypowerwhen:(1)thecorrelations weare
faced with are, by themselves, mysterious; and (2) an identity would be a better
explanation of the correlations than competing explanations. Granted, it would take
some work to show that (1) and (2) obtained for any given example—but their
possibility shows that identity claims might still be ‘‘in the running’’ as explanations
of particular mind-brain correlations.
The main point of this paper is not to argue against Kim, however. I am taking it
as an assumption that it is at least plausible for an identity claim to be part of an
explanation as to why some M and some B are correlated. Such correlations are
themselves summaries of patterns of observation. Thus identity claims must be able
to explain the systematic pattern of observations we obtain, and do so better than
rival explanations. My main argument is that, in doing so, identity theory faces a
dilemma.
Although an identity claim could be a good explanation of a mind-brain
correlation (and thus also explain the patterns of observation we obtain), there are
many other ways in which a correlation can occur, ways that are consistent with the
results from experiments. To suggest some alternatives, consider that we would find
a correlation between a given mental state and some brain state because:
(1) The mentalstate caused thebrainstate;
(2) The brainstate caused thementalstate; or
(3) Both themental state andthebrain state arisefrom a commoncause.
These relations would still yield mind-brain correlations, and yet the mental state
and brain state would not be type-identical.11
In what follows, then, I will lay out a particular example where one would expect
an identity claim to hold: that of the correlation between thirst and hypothalamic
activity. What a detailed examination of this case will show is that, even here, the
correlation between thirst and hypothalamic activity is not as strong as needed to
fullysupportanidentityclaim—otherrelationscouldexplainthecorrelationaswell.
5. A Historical Case: The Hypothalamus and Thirst
ThecaseIwanttoexploreisoftenconsidereda‘‘classictextbookcase’’ofmind-brain
correlation: the correlation between the activity of the hypothalamus and the
sensation of thirst. What Iwant to showwith this case isthat, once one explores the
details,evenaseeminglystrongcorrelation(and,hence,agoodcaseofamind-brain
claim) turns out to be a relatively weak correlation—and so the third premise of
Hill’s argument is false for many cases of mind-brain correlation.
Philosophical Psychology 193
The hypothalamus is a cluster of structures located near the brain stem between
the pituitary gland and the thalamus, surrounding the third ventricle of the brain.
It is densely connected with a number of areas, including prefrontal cortex,
hippocampus, amygdala, pituitary, and the brainstem. Since at least the 1950s,
experimenters have suspected that the hypothalamus plays a pivotal role in the
regulation of thirst. Because part of the hypothalamus lies outside the blood-brain
barrier, it is ideally situated to receive blood-borne messengers. Its dense intercon-
nections with the pituitary also make it well situated to control the internal
environment. Indeed, the received view is that the hypothalamus, or parts thereof,
is ‘‘the center’’ of our thirst sensations.12
Why is the hypothalamus a good test case for the claim that a mind-brain
correlationisevidenceforanidentityclaim?Therearethreethingsthatmakethisan
appropriate case to study. First, the hypothalamus is an evolutionarily old structure.
Itisfoundinseveralspeciesandseemstohavechangedlittleoverevolutionarytime,
making it comparable across species (compared to, say, parts of neocortex).
Second,thehypothalamusseemstobeinvolvedinanumberof‘‘drives’’whichare
relatively easy to study: hunger, thirst, sexual response, fear, etc. Whereas the
behaviorswewouldexpectfrom, say,avisualsensation may varyfromindividualto
individual, the behaviors that arise from drives are especially stereotyped. Thus we
havegoodwaysofdetectingthirst:wecanmeasuresuchthingsasmovementtowards
water, amount of water drunk, number of drinking episodes, etc.
Third, we know a great deal about the chemistry and physiology of the
hypothalamus. We know what neurotransmitters it traffics in, and we know what
chemicalchangesinthebodytendtoaffectit(forexample,seeRolls&Wood,1977).
This gives us the ability to both manipulate and measure this structure.
Sothe hypothalamusseems arather goodcandidate forthekind of IBEargument
I have been considering. We have methods to influence the activity of the
hypothalamus,andwealsohavegoodmethodsforinducingorslakingthirst.Wealso
have good ways of operationalizing thirst—i.e., there are a number of behaviors we
can measure that depend directly on thirst (such as movement towards water,
amount of water drunk, number of drinking episodes, etc.). And given that the
hypothalamus exhibits little variation across individuals and across species, we have
a number of animal models we can use to test hypotheses.
The first critical experiments that correlated the hypothalamus with thirst were
done in the 1950s by Andersson and colleagues (Andersson, 1953; Andersson,
Dallman, & Olsson, 1969; Andersson & McCann, 1955; Greer, 1955). These early
experimentsshowedthatinjectionsofhypertonicsalineinthehypothalamusofgoats
eliciteddrinking,evenintheabsenceofotherfactors(lowbloodosmolalityandhigh
body temperature, for example). Greer (1955) and Mogensen and Stevenson (1967)
went on to show that electrical stimulation of the lateral part of the hypothalamus
alsoinduceddrinking.Thesestudiesshowthatactivatingaparticularbrainstatelead
totheexpressionofbehaviortypicalofbeinginacertainmentalstate—beingthirsty.
In the symbolization from above, these studies establish that B!M.
194 B. N. Towl
Further studies showed that lesioning parts of the hypothalamus in rats and cats
often extinguished drinking behavior (Bellinger, 1987; Cambiasso & Chiaraviglio,
1992; Clark et al., 1991; Saad, Luiz, De Arruda Camargo, Renzi, & Manani, 1996).
OnestudydonebyCareyandGoodall(1975)showedthatlesionstomedialpreoptic
areaofthehypothalamusinratsloweredtheir‘‘tolerance’’forwateradulteratedwith
quinine, suggesting that their thirst drive was having less of an effect on behavior.
These studies are consistent with (cid:2)B!(cid:2)M.
Studies have also been done altering the mental states of animals and looking for
changes of brain state. Patronas, Horowitz, Simon, and Gertsberger (1998), for
example, did a series of experiments that induced thirst in rats by dehydration and
heat acclimation. They then noticed an increase in the expression of the c-fos
protooncogene, which suggests that hypothalamic activity increases during long
exposure to thirst inducing stimuli. Other labs have shown that the mere visual
presentation of a known water source (a drinking syringe, for example) increases
hypothalamic activity (Rolls & Rolls, 1982). Thus manipulations of the mental state
cause noticeable changes in the activity of the hypothalamus: M!B.
These studies nicely mirror the criteria I set out above in section 3.13 It is because
of these and similar studies that many researchers consider the hypothalamus a
‘‘thirst center’’ in the brain, involved in the regulation and control of drinking
behavior.Butsubsequentresearchshowsthatthestoryhereisnotsoclear-cut:there
are several problems with the ‘‘hypothalamus as thirst center’’ story.
First, there seem to be conflicting data about which part (or parts) of the
hypothalamuscountas‘‘thecenter.’’Thedorsalmedialnucleusofthehypothalamus
seems a likely candidate, since lesioning this area reduces drinking behavior
(Bernardis, 1970; Bernardis & Bellinger, 1998; Clark et al., 1991), and electrical
stimulation causes drinking (Rolls & Rolls, 1982). But lesioning this area often also
reduces eating behavior, and both behaviors tend to recover spontaneously
(Rowland, 1976; Zigmond & Stricker, 1973; also see the debate covered in Wayner,
1964).Thusitisnotclearthatthedorsalmedialhypothalamusisresponsiblejustfor
thirstbehavior,norisitanecessarycomponentinsomecases.Forotherareasofthe
hypothalamus, the story seems to be the same: there doesn’t seem to be one area
singly responsible for, or primarily dedicated to, thirst related activity.14
Second, thirst related behavior can be elicited through activation of brain areas
outside of hypothalamus. A series of studies have showed that activating the
ventrolaterialperiaqueductalgraymatter(orPAG—apartofthebrainstem)ofcats,
rats, and monkeys causes many of the same thirst-related behaviors as activation of
the hypothalamus (Wyrwicka & Doty, 1966; Sharpe & Swanson, 1974; Swanson &
Sharpe, 1973). Likewise, lesions in this area cause the loss of drinking and feeding
behavior, just as lesions of the DMH do (Lyon, Halpern, & Mintz, 1968). There is
evenevidencethatactivatingpartsoftheneocortexofmacaquemonkeys(specifically
area32inmedialprefrontalcortex)elicitsdrinkingbehavioraswell;similarfindings
have come out of PET studies of human brains (Denton et al., 1998, 1999). Also
playing key roles are mesial cortex and thalamus (Sewards & Sewards, 2003) and
medial forebrain (Rundgren & Fyhrquist, 1978). Granted, these other areas are
Philosophical Psychology 195
connected to the hypothalamus. But they show their own correlations with drinking
behavior in a way that throws doubt on the identity claim.
Third,aseriesofexperimentsbyRollsandcolleagues(Rolls,1974;Rolls,Burton,&
Mora, 1980) showed that some hypothalamic neurons in monkeys increased their
activity with the taste of water in the mouth, as compared to isotonic saline, and
decreased activity when a puff of dry air was presented. Thus, manipulations that
increase the satiation in monkeys cause increased activity, while manipulations that
cause thirst sometimes cause decreased activity. We would expect the opposite
pattern of results if activity in the hypothalamus represented thirst.
Thesethreeconsiderationscastsomeseriousdoubtontheclaimthatactivityinthe
hypothalamus, or parts thereof, are identical with the sensation of thirst. Although
the correlation looks quite strong at first, there are several experiments that show
that: (1) multiple other areas produce thirst responses; (2) the hypothalamus is
responsible for more than just thirst; and (3) lack of hypothalamic activity does not
always correlate with lack of thirst.
This is not to say that there is no correlation between hypothalamic activity and
thirst. The initial findings of these researchers show some correlation. The problem
is simply that the correlation is not a maximally strong one.
Sowhatdoesthehypothalamusdowithregardstothethirstmechanism,ifitisnot
the ‘‘center’’ for our thirst sensations? There are at least two likely theories worth
exploring.Oneisthatthefunctionofthehypothalamusmightbetomonitorcellular
dehydration via blood osmolality, and ‘‘kick-off’’ various thirst mechanisms in
response.Onthistheory,althoughtheactivityofthehypothalamusisnotidenticalto
the sensation of thirst, it regularly causes the sensation of thirst. A second theory
(Rolls & Rolls, 1982) is that the hypothalamus is a kind of ‘‘reward center’’ for
successful eating and drinking behaviors. Again, this would make the activity of the
hypothalamus not identical to the sensation of thirst, but it would be caused by the
satiationofthirst.Thesetworelations—bothcausalrelations,bytheway—seemtofit
the evidence better than the relation of identity. Given this, the correlation between
thirst and hypothalamic activity is not best explained by the thesis that one is
identical to the other.
Theseresultsarenotspecifictothegivenexample.Wheneverwehavealess-than-
strong correlation, it will be possible that another relation besides identity could
explainthecorrelationwefind.Thisisnottosaythatnomentalstatewillbefoundto
be identical to any brain state. But, for there to be an IBE argument for such an
identity claim, there would have to be a maximally strong correlation.
6. The Dilemma
For Hill’s argument above to work, then, the PPC must capture not just any
correlationsbetweenmentalstatesandbrainstates;rather,itmustcapturemaximally
strong correlations. Otherwise, the third premise of the argument would be false for
many cases. The hypothalamus case is one example of this. The case illustrates a
196 B. N. Towl
general principle, however: the weaker the correlations one considers, the more
cheaply they can be had. Identity claims, however, are strong claims. Thus the
numberofidentitiesisboundtobemuchsmallerthanthenumberofcorrelationswe
uncover. So not all correlations can be evidence for an identity.
So suppose we take the set of correlations to include maximally strong
correlations. If we insist that a correlation be sufficiently strong to support an
identityclaim,wewillfindthatthenumberoftrulystrongcorrelationsisvanishingly
small in neuroscience. To cite some anecdotal examples:
. Some neuroscientists claim that there are facial recognition cells in inferotemporal cortex,
though there is evidence for this, these cells also become active when a toilet brush is moved
rapidly through theirreceptive fields (Gross,2008; Richmond &Wurtz,1982).
. Fearresponsesandfearconditioningdocorrelatewithamygdaleactivity,buttheamygdalaalso
seemstoplayrolesinlong-termmemoryconsolidation,theprocessingoffacialexpressions,and
detectionof‘‘personalspace’’violations(Kennedy,Gla¨scher,Tyszka,&Adolphs,2009;Williams
etal.,2006).Furthermore,areassuchasthemedialgeniculatenucleus(MGN)arealsouniquely
poised to regulatefear responses (Weinberger, forthcoming).
. Though anterior cingulate activation seems to correlate well with response selection, error
detection, and emotional salience, there are a number of studies contradicting these roles
(Fellows &Farah,2005; Nachev, 2006; Rushworth,Behrens, Rudebeck, &Walton, 2007).
Space limits me from going into detail about these further cases, but we can
explain their occurrence—and the possibility of many such others—straightfor-
wardly. Our mental taxonomy is not devised solely on the basis of neuroscientific
evidence. Mental categories might well come from folk psychology, older-but-still-
popular psychological theories, current theories in psychology, or psychiatry, or
anthropology, or sociology, etc. Given the diversity of sources for our mental
categories, we would expect many cases where a given mental category does not line
up neatly with our neuroscientific categories.
Ifthisiscorrect,thereareboundtobemany examplesofweakcorrelations inthe
neuroscience literature. This creates a problem for the induction needed for Hill’s
argumenttowork.IfonlystrongcorrelationsgiveusanIBEargumenttoanidentity
claim, there will be very few identity claims. And so the general thesis, that type-
identity theory is true for all or most mental states, will be an induction based on an
exceedingly small number of cases. So we still have a very unconvincing positive
argument for the type identity theory.
7. Objections and Implications
TherearesomereadyobjectionstotheargumentIhavegivenhere;tomakemycase,
there are three that I need to address. The first objection is that I have focused only
on correlations that have seemed strong but that are, in fact, weak. The second
objectionisthatIhavefocusedonneuralareasthataretoosmall.Thethirdobjection
is that I have focused on a largish brain area, rather than smaller network or