Generous or Parsimonious Cognitive Architecture? Cognitive ...Generous or Parsimonious Cognitive...

Brit. J. Phil. Sci. 59 (2008), 121–141

Generous or ParsimoniousCognitive Architecture? CognitiveNeuroscience and Theory of Mind

Philip Gerrans and Valerie E. Stone

ABSTRACT

Recent work in cognitive neuroscience on the child’s Theory of Mind (ToM) has pursuedthe idea that the ability to metarepresent mental states depends on a domain-specificcognitive subystem implemented in specific neural circuitry: a Theory of Mind Module.We argue that the interaction of several domain-general mechanisms and lower-leveldomain-specific mechanisms accounts for the flexibility and sophistication of behavior,which has been taken to be evidence for a domain-specific ToM module. This findingis of more general interest since it suggests a parsimonious cognitive architecture canaccount for apparent domain specificity. We argue for such an architecture in twostages. First, on conceptual grounds, contrasting the case of language with ToM, andsecond, by showing that recent evidence in the form of fMRI and lesion studies supportsthe more parsimonious hypothesis.

1 Theory of Mind, Metarepresentation, and Modularity2 Developmental Components of ToM3 The Analogy with Modularity of Language4 Dissociations without Modules5 The Evidence from Neuroscience6 Conclusion

1 Theory of Mind, Metarepresentation, and Modularity

In 1985, Simon Baron-Cohen, Alan Leslie, and Uta Frith published aninfluential paper entitled ‘Does the autistic child have a theory of mind(ToM)?’ They presented evidence that children with autism were impairedrelative to typically developing and Downs syndrome children on nonverbal‘false-belief’ tests of ToM, the ability to form beliefs about the mentalstates of others. Recently, some researchers in cognitive neuroscience haveargued, on the basis of neuroimaging results, that the temporoparietal

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122 Philip Gerrans and Valerie E. Stone

junction (TPJ) contains a domain-specific cognitive system specialized forToM. This suggests an elegant theoretical and empirical marriage betweendevelopmental psychology and neuroscience. The basis of this marriageis the idea that cognitive neuroscientists and developmental psychologistsare studying the same domain-specific ‘module’ at different levels; withneuroscience revealing the neural substrate of a discrete cognitive capacity.1

We argue, however, that both fields are studying the emergent outcome ofinteraction between numerous domain-specific low-level cognitive systemsand domain-general cognitive systems. The low-level domain-specific systemssuch as joint attention, gaze tracking, animacy detection, and recognition ofemotional expression develop early (Baron-Cohen [1995]; Rutherford et al.[2006]; Stone [2005]). The domain-general systems such as metarepresentation(MR), secondary representation (SR), executive function (EF), recursiveembedding, and natural language develop later (Perner [1991]; Suddendorf[1999]; Suddendorf and Whiten [2001]; De Villiers and Pyers [2002]; Smithet al. [2003]). It is their interaction in development, rather than the maturationof a mindreading module, which explains the emergence of ToM. Thus thenotion of ‘modularity’ of ToM is misleading if taken to mean a discretecognitive entity implemented in specialized neural circuitry.

The argument against the presence of a ToM module (or a ToM domain-specific cognitive mechanism) provides a general lesson for the explanation ofcognition and a cautionary tale for evolutionary psychology: modulae non suntmultiplicanda praeter necessitatem. We develop the argument in five stages:

1. Passing the false-belief test does not necessarily depend on adomain-specific cognitive mechanism. We suggest an alternativecognitive architecture that can explain the phenomena that led tothe postulation of the ToM module.

2. Recent evidence from neuroscience does not support the inference tothe presence of a ToM module.

1 If so, we would have identified a cognitive device evolved to solve an adaptive problem (Sterelnyand Griffiths [1999]). Evolutionary psychologists suggest we identity such devices in order toassist in determining which features of the cognitive phenotype are adaptations (Tooby &Cosmides [1992]). Atkinson and Wheeler ([2004]), however, point out that the relationship ofexplanatory priority between cognitive device and adaptive function is theoretically problematic.Although many of Atkinson and Wheeler’s arguments are situated within the framework ofevolutionary psychology, rather than developmental psychology and neuroscience, we aresympathetic to a general line of argument used by critics of naıve adaptationism. The inferencefrom apparent cognitive structure in the phenotype (in our case a dissociation in performanceon false-belief and false-photo tasks) to the presence of domain-specific cognitive mechanismsis not straightforward. Just as Samuels ([1998]) proposes an alternative general processingarchitecture (the library conception) to argue against the inference from apparent domainspecificity to modularity, we provide a specific alternative architecture to show that the selectiveactivation in the TPJ in ToM tasks is not evidence for the presence of a domain-specific cognitivemechanism.

Generous or Parsimonious Cognitive Architecture? 123

3. Our suggested architecture is more parsimonious.

4. We support our case in part by comparison to the case of language,which many theorists argue is a high-level module, which takesoutputs from domain-specific cognitive subsystems as inputs. Theinterest of the case of language is that if those arguments are soundthen we have a case of a module constructed in development bythe type of interaction we think explains ToM. We argue, however,that the arguments in support of modularity of language do notapply to the case of ToM. This is particularly important because thecase of language acquisition has served as a general model for thepostulation of domain-specific cognitive architecture (Pinker [1989];Cosmides and Tooby [1995]; Cosmides and Tooby [1994]; Gelmanand Hirschfeld [1994]).

5. Thus, activation in TPJ revealed in fMRI studies does not reveal theneural substrate of a ToM module. In fact, TPJ may help implementa domain-general cognitive capacity, MR. This result would beconsistent with the explanation of ToM proposed by Baron–Cohen,Leslie and Frith 20 years ago.

Before developing our argument we need to discuss a central distinctionbetween domain-specific and domain-general cognitive abilities. Domain-general abilities include working memory, EF, recursion, attention, and MR.These capacities process information without being restricted to a particularrepresentational format. While the visual system, for example, can process onlyoptical information, attention can be focused on visual, auditory, sensory,spatial, or higher-order representations produced by any more-specializedsystem. The same is true of EF (inhibition, sequencing, flexible controlof attention): any of these processes must operate over a wide variety ofrepresentational formats.

Domain-specific subsystems, such as the visual system, process only theirproprietary inputs using representations specialized for their task and pro-duce outputs in specialized representational formats. It is this specializationthat provides the contrast between domain-general and domain-specific cog-nitive systems. Indeed, the lack of specialization of domain-general systems isrequired in order for them to be able to process the variety of representationsproduced by the mind’s domain-specific systems. The existence of domainspecificity necessitates domain generality for any creature that needs to inte-grate different types of information. The terms domain-specific and modularare sometimes used interchangeably; however, the notion of a ‘module’ is acontested one. For example, it has been variously characterized as a restricteddatabase, a specialized neural mechanism, distributed or localized, an infor-mationally encapsulated cognitive process, a cognitive process vulnerable to


selective deficit, a functionally discrete component of a computational system,or a content-specific cognitive capacity.2 The advent of fMRI has led mostresearchers in the field to adopt one of these conceptions of modularity toexplain the selective activation of different neural circuits observed underdifferent task conditions: that is, to treat neural activation as implementationof one of these definitions. It is worth noting that all these characterizationsof ‘module’ attempt to preserve the basic distinction between specializationand generality while doing justice to the complexity of cognition at differentlevels of analysis. We do not wish to adjudicate debates between proponents ofdifferent conceptions because the decision to adopt a definition depends verymuch on which aspects of cognition one wants to emphasize.3 For example,encapsulation theorists need to deal with the large amount of top-down pro-cessing, recurrence, and cross-talk in the brain, which means that few systemsare entirely informationally discrete. Localization theorists must address thedistributed nature of cognition, and so on. Each view seems to encountersome difficulties and counter examples. Nonetheless, despite the problem ofproviding a watertight definition, brain research continues (i) to demonstratea very high degree of functional specialization down to the molecular level; (ii)to show that some cognitive functions, such as attention or working memory,are not restricted in the representations they can take as inputs.

Consequently, we will use the terms domain-specific cognitive mechanismand domain-general cognitive mechanism to capture this distinction in our

2 (Coltheart [1999]) contains a helpful survey of costs and benefits associated with adoptingdifferent conceptions. As he points out, following Shallice ([1988]) neuropsychologists useacquired lesion to determine functional architecture without being committed to a strongernotion of anatomical modularity. He also points out that Fodor’s influential discussion didnot propose necessary and sufficient conditions for modularity but a cluster of related featuresmodules might possess in degrees. Like Pylyshyn ([1999]), however, Fodor does think thatmodules are informationally encapsulated from central processes of inference. Samuels ([1998])helpfully makes a distinction between the algorithmic conception and the hardware conceptionof modularity. A laptop is a domain-general piece of hardware, which runs many domain-specific programs (e.g. a word processor and an internet browser). If hardware is domain-specificthen the algorithms running on that hardware must also be domain-specific. This is the intuitiveidea behind the idea that a neurally specialized system (such as vision) is encapsulated fromdomain-specific processes advanced in the work of Fodor ([1983]). But it does not followfrom the fact that algorithms are domain-specific (e.g. a graphics program), that hardwareis domain-specific. So the inference from the presence of domain specificity in the cognitivephenotype to domain specificity in the neural phenotype is invalid.

3 Atkinson and Wheeler ([2004]) point out that the possibility of different foci of explanationgenerates a problem of indeterminacy for the boundaries of modules. Like Samuels, their targetis the use of adaptationist methodology to determine the boundary or domain of a module.Which of an organism’s features (cognitive or physical) is an adaptation requires us to solve asimultaneous equation with variables being the adaptive problem and the feature (Sterenly andGriffiths [2003]). Since both features and adaptive problems decompose into microconstituentsthe problem of indeterminacy rapidly ramifies. As they point out, this does not invalidate theprogram of linking neural and cognitive specialization, but it requires the theorist to move‘within and between levels of organization and levels of analysis’ (p. 170). Our tour of thisterritory did not reveal any evidence of either hardware or algorithm specialized for ToM.


discussion. This is adequate for our purpose, which is to recapture the insightof the original proposal by Baron-Cohen et al. ([1985]) that ToM is theapplication of a domain-general capacity to a specific task.

In their 1985 paper, Baron–Cohen, Leslie & Frith proposed a cognitiveaccount of ToM which treats it as ‘one of the manifestations of a basicmetarepresentational capacity’ ([1985], p. 37, emphasis added). MR is theability to represent the relationship between a representation and its object. Asthe quote implies it is not necessarily limited to MR of mental states (Perner[1991]; Suddendorf [1999]; Suddendorf and Whiten [2001]; Corballis [2003];Povinelli [1996]) and is thus a domain-general ability. Subsequently, otherdevelopmental theorists pursued the idea that ToM depends on a domain-specific capacity for MR of mental states: the ToM mechanism (e.g. Leslie[1987], [1994]). Theorists differ over the nature of domain specificity in ToM.All agree ToM is content specific (its domain is the MR of mental states) but thenature of its representational format, relationship with other domain-specificcapacities, and neural implementation are controversial.

Evidence for domain specificity in ToM is provided by an apparentdissociation between domain-general MR and MR of mental states. Inparticular, many children with autism who fail the false-belief test pass thefalse-photograph test, which requires MR of representational relationshipswith nonmental state content, while normal children exhibit a converse patternof performance (Zaitchik [1990]).

For domain-specific theorists, ToM is a domain-specific capacity, andautism results from impairment to the development of a ToM mechanism:a neurocomputational system specialized for the MR of mental states. Thefact that autism is a developmental rather than an acquired disorder alsosuggests to some theorists that the domain-specific mechanism is innate, in thesame way that disorders such as specific language impairment support nativistinferences about the nature of human language ability. Although the coherenceof nativism and the inference from developmental deficit to innateness havebeen contested (Elman et al. [1996]; Karmiloff-Smith [1998]; Karmiloff-Smithet al. [2003]), those supporting the domain-specific conception of ToM regardit as a domain-specific cognitive adaptation that depends on the geneticallyguided maturation of specialized neural circuitry. It is for this reason that thenear-universal presence of ToM in the human phenotype has been recruited byEvolutionary Psychology as evidence for domain-specific nativism (Cosmides& Tooby [1995]).

More recently, cognitive neuroscience, using data from fMRI and lesionstudies, has investigated ToM by locating neural circuitry which subserves itand attempting to distinguish ToM from other capacities, such as workingmemory or more general inferential abilities (Stone et al. [1998]; Saxe &Kanwisher [2003]; Apperly et al. [2004]; Samson et al. [2004]; Saxe et al. [2004]).


Initial studies focused on the frontal lobes, either medial prefrontal cortex(MPFC) (Fletcher et al. [1995]; Gallagher and Frith [2003]) or orbitofrontalcortex (OFC) (Stone et al. [1998]; Gregory et al. [2002]). More recent studieshave implicated the TPJ in ToM performance. The TPJ is of particular interestbecause fMRI studies showed it to be active during false-belief tasks butnot false-photograph tasks, suggesting a neural substrate for the behavioraldissociation that prompted the initial postulation of a ToM module (Saxe andKanwisher [2003]; Saxe [2004]).

These convergent lines of inquiry from developmental psychology and neu-roscience have persuaded many theorists that ToM is a domain-specific cogni-tive ability. However, we argue that an alternative model of ToM developmentcan account more parsimoniously for the data from autism and neuroscience.

Our main concern is to defuse the arguments for domain specificity inToM rather than nativism, since the two are logically independent. However,the inference to nativism from empirical evidence about ToM is less persua-sive once the relationships between developmental components of ToM areclarified.

2 Developmental Components of ToM

Before we consider the evidence from neuroscience let us recall what is incommon between all theorists of ToM development. First, development ofToM depends on the prior development of a suite of specialized lower-level cognitive mechanisms. These precursor mechanisms represent vitalinformation about the social world of the infant and toddler, and mediate herearliest interactions with others. These mechanisms enable face processing,representations of gaze direction, gaze monitoring, detection of animacy,tracking of intentions and goals, and joint attention (Baron-Cohen [1995];Dawson et al. [1998]; Crichton and Lange-Kuttner [1999]; Woodward [1999];Charman et al. [2000]; Hare et al. [2000]; Carpenter et al. [2001]; Csibra et al.[2003]; Saxe et al. [2004]; Schultz [2005]; Stone [2005]; Rutherford et al. [2006]).These capacities seem to be specific to social stimuli, are shared with otherprimates, and appear to depend on neural circuitry that responds specifically tosocial stimuli (e.g. Campbell et al. [1990]; Kumashiro et al. [2002]; Blakemoreet al. [2003]; Csibra et al. [2003]; Povinelli et al. [2003]). Gaze monitoring, forexample, seems to involve specific regions of the superior temporal sulcus thatrespond to the stimulus of eye gaze direction but not to other stimuli, even otherstimuli that are physically similar to images of eyes (Campbell et al. [1990];Perrett et al. [1990]; Hoffman and Haxby [2000]). Assessing others’ goals andintentions seems to depend on specific representations of certain movementpatterns, limb movement, combined with gaze, head or body orientation, and


involves both superior temporal sulcus and superior parietal and lateral frontalareas (Jellema et al. [2000]; Blakemore et al. [2003]).

The development of these domain-specific mechanisms ensures that thenormal toddler is equipped with a sophisticated battery of mechanisms, whichenable her to negotiate the social world on the basis of perceptually availableinformation. In this respect, she is like the great apes and uses essentiallythe same cognitive equipment. Like the great apes she cannot computeover abstract representations of unobservable states to predict and explainconspecific behavior. She cannot metarepresent beliefs (Suddendorf [1999];Suddendorf and Whiten [2001]).

Thus, one way to describe the issue between domain-specific and domain-general accounts of ToM abilities is as a debate about the nature of animportant cognitive difference between the great apes and ourselves. Weargue that homo sapiens’ superior ToM capacity does not depend on theevolution in the hominid line of a domain-specific ToM mechanism. Ourdomain-general capacities in combination with domain-specific precursors,such as gaze processing and emotion recognition, explain ToM performance.

The presence and nature of these domain-general capacities is anotherpoint of agreement between all theorists. The normal 4-year-old isequipped with a battery of cognitive devices which subserve domain-generalmetacognitive computational functions. Advanced EF (meaning workingmemory, inhibition, and flexible control of attention), SRs (the capacity tohold in mind and compare two different representations), recursion (theability to compute embedded representations), and MR (understandingthe representational nature of the relationship between representation andreferent) have all come online by ages 2–4, though they may continue todevelop further after age 4 (Perner [1991]; Suddendorf [1999]; Suddendorf andWhiten [2001]; De Villiers and Pyers [2002]; Smith et al. [2003]). It is advancedEF, MR and recursion–all domain-general cognitive abilities–that distanceus from our primate ancestors (Suddendorf [1999]; Suddendorf and Whiten[2001]), rather than the fact that we possess a domain-specific ToM mechanismand they do not.

However, our claim is not that presence of ToM in normal children, orits absence in autism, is entirely accounted for by these metarepresentationalabilities. Toddlers, chimps, and children with Downs syndrome, who lackmetarepresentational abilities in different ways and to different degrees, donot resemble individuals with autism. Further evidence is the fact that althoughsolving false-belief tasks clearly places demands on EF, there are no clear earlydeficits in EF in autism (Griffith et al. [1999]). Furthermore, apparent deficitsin EF disappear when children with autism are tested by a computer ratherthan a person (Ozonoff et al. [1991]; Ozonoff [1995]).


In our view, these results are to be expected since ToM abilities depend, noton MR, EF, language, or recursion per se, but on their developmentalinteraction with the low-level precursors previously described, e.g. gazeprocessing, emotion recognition, and joint attention (see Figures 1 and 2 for agraphic representation of this architecture in comparison to that postulated bymodular explanations of ToM). The result of this interaction is not the creationof an extra module but the wiring up of distributed metarepresentationalcircuitry which can take social information as input (Gerrans [2003]; Stone[2005]) and, ultimately, compute over abstract representations of mentalstates not tied to a perceptual modality. The manipulation of those abstractrepresentations is not, however, essentially different from the manipulation ofother abstract representations involving recursion, natural language, and MR.Nor does it need to involve a distinct neurocomputational mechanism.

MR operating on information about eye gaze and attention (who saw orwas attending to what) allows us to represent others’ knowledge states (whoknew what) (Baron-Cohen [1995]). Recursion operating on MRs of mentalstates allows us to reason about not just others’ thoughts, but others’ thoughtsabout thoughts (Corballis [2003]). Indeed, children’s abilities to use embedded

Figure 1. Mental state inferences with a TOM module.


Figure 2. Mental state inferences without a TOM module.

syntactical structures comes online shortly before the ability to solve false-belief tasks, supporting the view that recursion may be a general ability servingboth tasks (Apperly et al. [2004], [2005]). EF allows us to keep the elementsof a social interaction in mind, and inhibit our own knowledge of the state ofreality when asked what someone else’s mental state is (Stone [2005]). Bothworking memory and inhibition have been shown to be related to performanceon ToM tasks (Keenan [1998]; Stone et al. [1998]; Carlson and Moses [2001]).We note in this regard, that Sabbagh et al. ([2006]) found that 3–5-year-oldperformance on an executive task requiring inhibition predicted performanceon false-belief and false-sign tasks but not false-photo tasks. In summary,deficits on ToM tasks could potentially result from deficits in either low-levelinput systems (e.g. joint attention) or higher-level domain-general capacities,rather than in a separate ToM mechanism.

3 The Analogy with Modularity of Language

Our view seems to face two related problems. The first is that a modulartheorist could point out that maturation of any cognitively sophisticatedmodule would require developmental interaction between domain-general


cognition and domain-specific precursors. In the case of language, for example,domain-specific mechanisms such as phonological processing interact withdomain-general ones such as EF, SR, and MR and the consequence of thisinteraction is the construction of a language module (Smith [1999]; Saxeet al. [2004]), which is vulnerable to both developmental and acquired doubledissociations. In fact, the case of language is instructive because when wecompare language and ToM we find that the main arguments for domainspecificity between the two cases are not analogous. Our discussion is briefbecause we are conceding the controversial points that language is modularand that Specific Language Impairment is a developmental dissociation of thatmodule. We merely point out that arguments for those conclusions are muchless persuasive in the case of ToM.

First, Poverty of Stimulus arguments for modularity of language rely onthe fact that the evidence available to children in their linguistic environment(primary linguistic data) underdetermines possible grammars. In order toexplain the near-universal convergence of developmental trajectories acrossthe human cognitive phenotype we need to postulate specialized cognitivearchitecture (Chomsky [1986]). The inference to ToM from the child’sexperience, however, is not similarly unconstrained. The child’s domain-specific precursors to ToM are a rich body of evidence for the hypothesis thatother people act on the basis of intentional states. The child does not need aspecial neurocomputational device to generate and test that hypothesis, shemerely needs to apply her domain-general capacities for hypothesis formationto the ‘primary psychological data’ in which she is immersed.

Second, the theoretical argument for language modularity is empiricallyreinforced by the presence of acquired dissociations, such as aphasia, in whichsyntactic processing is impaired while both domain-specific precursors tolanguage and domain-general mechanisms remain intact. However, there areno equivalent cases of acquired deficits to ToM that spare other cognitiveabilities (see Section 5 for a full discussion of recent neuroscientific workon this issue). If ToM is a genuine domain-specific mechanism, this lack ofempirical evidence is surprising.

Third, the modular theorist of language can point to cases of developmentaldouble dissociation of the capacity for syntactic processing. Smith andIanthi–Simpli ([1995]) report the case of a quite severely cognitively impairedman who, nonetheless, has an amazing facility with the syntactic aspects of overtwenty languages. This man’s facility with syntax could be explained by thesparing of his language module. His case, however, is only a single dissociation,of spared syntactical abilities from impaired domain-general cognition. Doubledissociations are more convincing arguments for modularity, and the reversedissociation is in fact known. There are cases of selective impairment tosyntactic processing with sparing of other cognitive capacities: the disorder


known as Grammatical Specific Language Impairment is interpreted in thatway. (Gopnik and Goad [1997]; Van der Lely and Stollwerk [1997]).

Whether autism is evidence for the presence of a selective developmentalsingle dissociation in a ToM module is still at issue, as discussed below.However, there is no evidence for a double dissociation, the selective sparing indevelopment of ToM. Researchers were initially misled by the hypersociabilityand expressiveness of children with Williams syndrome into thinking thatthey had a spared ToM (Karmiloff-Smith et al. [1995]) However, subsequentstudies have shown that their ToM also develops abnormally, as do theirlanguage abilities (Tager-Flusberg [2000]; Gerrans [2002]). In our view, thisconnection results from the fact that language and ToM both depend onsome of the same domain-general capacities, MR and recursion, which maybe impaired in Williams syndrome.

Thus, the theoretical and empirical considerations which support modularitytheses about language do not apply straightforwardly to ToM. The empiricalevidence in it is simply not there, as discussed further below, and the theoreticalarguments (poverty of the stimulus) are difficult to uphold in light of the socialinformation children are exposed to.

4 Dissociations without Modules

However, even if proponents of domain specificity in ToM accepted thesepoints, they would press a second difficulty for our account. We stillneed to explain dissociations between performance on false-belief and false-photograph tasks. This difficulty seems especially pressing given that attemptsto explain ToM deficits in terms of deficits in EF or MR have not been entirelysuccessful. Attempts to explain autism in terms of EF have foundered on alack of early EF deficits in autism, and attempts to explain it as a generalmetarepresentational deficit have foundered on autistic children’s excellentperformance on false-photograph tasks.

Our reply to domain-specific theorists of ToM is that if children withautism have intact MR, but impaired inputs to MR from impaired low-level domain-specific mechanisms (e.g. joint attention), then one wouldpredict exactly this dissociation between false-photograph and false-beliefperformance. Individuals with autism perform well on the false-photographtask because the inputs to the metarepresentational system, in that task, arenot impaired in autism. See Figure 3 for a graphic representation.

We believe that deficits on ToM tasks in autism arise essentially from deficitsin lower-level input systems. Research on social deficits in autism has shownclearly that children with autism have deficits in many early domain-specificsocial competences: face recognition, facial expression recognition, processingof gaze direction, and joint attention; (Osterling and Dawson [1994]; Boucher


Figure 3. False photo inferences.

and Lewis [1992a]; Dawson et al. [1998], [2004a], [2004b]; Klin et al. [1999];Baird et al. [2000]; Grice et al. [2005]; Schultz [2005]). The performance ofchildren with autism on ToM tests can be explained more parsimoniously bythe view that they have deficits, not in MR, but in lower-level domain-specificmechanisms for processing social information. Without proper inputs, theintact capacity for MR by itself cannot make correct ToM inferences with thesame fluency and automaticity as the mind of the normal 4-year-old. Thus, weargue that autistic deficits on ToM tasks are evidence, not for impaired MR,but are instead evidence of impaired inputs to metarepresentational systemsrecruited by ToM tasks. Strong evidence against this view would be a case ofan individual with specific deficits on metarepresentational ToM tasks, suchas false belief, but no lower-level social deficits, but as we noted, no such casehas been reported.

In our view, then, there should be cases of high-functioning autism spectrumdisorder (ASD) individuals in whom MR is intact. Evidence supports this view.In the absence of comorbid intellectual disability, individuals with autism seemto have intact capacities for MR, recursion and EF. Children with autismperform well on a nonmental metarepresentational task, the false-photographtest (Leslie and Thaiss [1992]). Baron–Cohen et al. ([1999]) report three cases


of high-functioning individuals with ASD, a mathematician, a physicist, and anengineering student. All three fields require people to represent the relationsbetween symbols and their objects (magnitudes, abstract spatial relations)and to perform recursive computations over these symbols. These three menexcelled in their fields (in fact, the mathematician was a Fields medalist),showing that their capacity for MR and recursion was intact. Furthermore,all did well on the Tower of Hanoi, an EF test that requires not onlyEF, but also recursion. However, all three had difficulty in inferring whatsomeone was feeling, or paying attention to, from pictures of the eye regionof the face (Baron–Cohen et al. [1999]), indicating a problem with lower-leveldomain-specific capacities for face and gaze processing rather than MR.

The weight of evidence indicates that the ToM impairments in autism andrelated disorders are a result of abnormal developmental interaction betweenlow-level input systems and higher-level domain-general capacities, causedessentially by deficits in ToM precursors. An individual with a deficit in ToMMR, without any deficit in lower-level social competences and without anymore general deficit in other relevant domain-general competences wouldprovide conclusive evidence against our view. No such case has yet beeninvoked in support of the domain-specific ToM hypothesis. Yet, as weremarked earlier, such cases of selective deficits are the core evidence formodularity hypotheses in other areas, such as language. We note in passingthat our view of the evidence is more parsimonious. The domain-specific ToMtheorist requires that MR emerges twice, once for mental states and once fordomain-general computation, in both evolution and development.

5 The Evidence from Neuroscience

If children with autism do not provide developmental evidence for domainspecificity in ToM, then perhaps data from neurological patients with lesionswould provide stronger evidence. These might provide evidence for selectiveacquired deficits to an existing domain-specific mechanism. In contrast, onour view, if deficits on ToM tasks result from deficits in higher-level domain-general capacities, rather than in a separate domain-specific mechanism, wewould expect ToM deficits to be accompanied by deficits in other tasksrequiring domain-general metacognition. Our prediction is vindicated byexisting evidence from neuropsychology. Current research seems only tosupport the view that it is not possible to be impaired on ToM tasks withouta concurrent deficit in either lower-level social abilities or deficits in otherdomain-general abilities.

Patients with OFC damage, for example, have been found to be impairedon ToM tasks (Stone et al. [1998]; Gregory et al. [2002]). However, they arealso impaired at recognizing facial expressions, judging mental states from eye


gaze or expression in the eye region of the face (Hornak et al. [1996]; Gregoryet al. [2002]; Snowden et al. [2003]). Furthermore, even their problems withsome ToM tasks may result from a difficulty in tracking intentions rather thanbeliefs (Stone [2000], [2005]). Thus, their mentalizing deficits can be explainedas a result of deficits in lower-level domain-specific mechanisms, not in higher-order domain-general mechanisms. Indeed, they can perform at ceiling-levelson false-belief tasks, even those requiring 2nd- and 3rd-order mental stateinferences (Stone et al. [1998]; Stone [2005]).

Early neuroimaging studies of ToM implicated the MPFC as an area neededfor the MR of mental states. If MPFC is necessary for ToM, then patientswith damage in that area should show specific deficits. However, patients withmedial frontal damage who have ToM deficits all have accompanying EFdeficits (Happe et al. [2001]; Gregory et al. [2002]; Stone [2005]). Furthermore,extensive medial frontal damage does not necessarily cause impairment inToM (Bird et al. [2004]). Hence, while MPFC is recruited during ToM tasksits contribution does not seem to be specific to ToM inferences.

Perhaps, then, more recent fMRI studies implicating the TPJ in theattribution of mental states might provide the basis for the ToM module?Saxe and Kanwisher ([2003]) found that the TPJ is more active in false-belieftasks than in tasks requiring the attribution of intention or social information.They also found that the TPJ was less strongly activated in false-photo tasksthan in false-belief tasks, which they say suggests a crucial role for the TPJin ToM inferences (Saxe and Kanwisher [2003]). However, in discussing theirresults, they also noted that while the false-photo tasks were ‘logically similar’to the ToM tasks they were also ‘more difficult’ (p. 1840). This raises thepossibility that the differential activation in TPJ is a resource artefact withinMR. That is to say, perhaps the difference in difficulty of the tasks accountsfor the difference in activation.

A possible explanation for the difference in difficulty is that theTPJ, although a domain-general metarepresentational system, is constantlyreceiving social information from the early domain-specific social input systemswe identified. Thus, the baseline level of activation for metarepresenting socialinformation is already high. Any new, nonsocial, task needs either to bring TPJactivation up to the same baseline or to inhibit the social input systems to allowthe nonsocial information to command TPJ processing resources. This couldexplain differences in activation levels in TPJ produced by false-belief andfalse-photograph tasks, and explain why Saxe and Kanwisher’s participantstook longer to do false-photograph than false-belief tasks.

Thus, more decisive evidence for TPJ specialization for ToM wouldbe provided by false-belief and false-photo studies, which posed identicalexecutive and cognitive resource demands. By using better-matched tasks in aneuroimaging paradigm, this issue could be resolved. The issue could also be


approached by further analyses of current imaging data. Saxe and Kanwisher([2003]) present contrasts between false-belief and false-photograph trials, andbetween false-belief task and nonmetarepresentational-task trials. They do not,however, present any whole-brain contrasts for all participants between false-photograph task and nonmetarepresentational-task trials. If such a contrastdid show differential activation in TPJ, then this would support the viewthat TPJ might underwrite MR more generally. In that case, the differentialactivation in TPJ between false-belief and false-photograph trials might simplyreflect how much each task demands of a metarepresentational capacity,though both require MR. In contrast, if TPJ was not differentially active whennonmetarepresentational tasks are subtracted from false-photograph tasks,there would be stronger evidence for TPJ’s specialization for belief state MR.

In the absence of imaging studies of false-belief and false-photograph tasksthat control for executive demands, we can turn to recent work with TPJ lesionpatients (Apperly et al. [2004]; Samson et al. [2004]). The hypothesis that TPJ isthe site of the ToM mechanism suggests that TPJ patients should have specificToM deficits. Indeed, initial research with TPJ patients showed deficits onfalse-belief tasks and not other EF tasks even when the general demands of EFwere controlled for (Apperly et al. [2004]; Samson et al. [2004]). However, themost recent research shows that all TPJ lesion patients who performed belowchance on false-belief tasks also performed poorly on a false-photograph test(Apperly et al., [2007]). Thus, there is as yet no conclusive evidence fromneurological patients that supports the claim that the TPJ is the site of adomain-specific mechanism dedicated to ToM inferences.

In fact, Apperly et al.’s data suggests that, although TPJ does not appearto be specialized for ToM, it may be specialized for MR and recruited bymetarepresentational aspects of ToM tasks.

6 Conclusion

As we noted earlier, MR is one of the abilities that emerged over the courseof hominid evolution that separates humans from the great apes, (Suddendorf[1999]; Corballis [2003]). In our view, it is not surprising that our ToM abilitiesemerge in concert with the suite of other abilities which distance us fromthe apes, all of which are essentially dependent on the architecture of theprefrontal cortex and temporal lobes. The fact that domain-general cognition,which allows us to detach from perceptual stimuli and represents unobservablefacts, is largely occupied in the first few years with social interaction is a naturalconsequence of our altricial developmental trajectory.

In the absence of strong evidence for dedicated neural circuitry or the disso-ciation of ToM from metarepresentational or lower-level deficits, it seems that


the interaction of several domain-general mechanisms and lower-level domain-specific mechanisms can account for the flexibility and sophistication of behav-ior which has been taken to be evidence for a domain-specific ToM module.

One can understand, as an episode in the history of science, why it seemednecessary to posit a specific ToM module. Early evidence from autism seemedto show a pattern of impairment in MR of belief, without a correspondingimpairment in MR in other domains (Baron-Cohen et al. [1985], Leslie andThaiss [1992]). Only later did it become clear that the deficits in autism were ata lower level. Furthermore, early explorations of the role of MR understood asa general prerequisite for higher cognition (Perner [1991]; Suddendorf [1999];Corballis [2003]) were overlooked once an apparent dissociation between ToMand domain-general MR was demonstrated (Leslie and Thaiss [1992]).

However, postulating a domain-specific ToM mechanism to explain autisticdeficits appears to have been an unnecessary elaboration on an alreadyadequate basic theoretical structure: i.e one containing domain-specific inputsystems like shared attention and domain-general systems such as EF, MR,SR, and language, for higher-order cognition. We believe that this episode inthe history of cognitive science can serve as a cautionary tale to evolutionarypsychologists and modular theorists: it is important, in proposing a certaincognitive architecture, to make sure that one has not postulated more modulesthan are warranted by the data: modulae non sunt multiplicanda praeternecessitatem. The data for language justifies the postulation of a separatemodule–not so for ToM. Just as the heliocentric theory of celestial motionremoved the need for epicycles in explanations of planetary orbits, a properunderstanding of the role of MR allows us to see past the limitations ofmodulocentric theorising about ToM.

Philip GerransDepartment of Philosophy

University of [email protected]

Valerie E. StoneDepartment of Psychology

University of [email protected]

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