Philip Gerrans

What's domain-specific about theory of mind?

Abstract Twenty years ago, Baron-Cohen and colleagues argued that autistic performance on false belief tests was explained by a deficit in metarepresentation. Subsequent research moved from the view that the mind has a domain-general capacity for metarepresentation to the view that the mind has a domain-specific mechanism for metarepresentation of mental states per se, i.e., the theory of mind mechanism (ToMM). We argue that 20 years of data collection in lesion patients and children with autism supports a more parsimonious view closer to that of the 1985 paper. Lower-level domain-specific mechanisms—e.g., tracking gaze, joint attention—interacting with higher-level domain-general mechanisms for metarepresentation, recursion, and executive function can account for observed patterns of deficits in both autism and neurological patients. The performance of children with autism or orbitofrontal patients on ToM tests can be explained more parsimoniously by their deficits in lower-level domain-specific mechanisms for processing social information. Without proper inputs, the intact capacity for metarepresentation by itself cannot make correct ToM inferences. Children with autism have no impairment in false photograph tests because their metarepresentational capacity is intact and they have no impairment in inputs required for such tests. TPJ patients have equivalent deficits on ToM and non-ToM metarepresentational tasks, consistent with a failure in domain-general processing. If deficits on ToM tasks can result from deficits in low-level input systems or in higher-level domain-general capacities, postulating a separate ToM mechanism may have been an unnecessary theoretical move.

A One-Stage Explanation of the Cotard Delusion

Cognitive neuropsychiatry (CN) is the explanation of psychiatric disorder by the methods of cognitive neuropsychology. Within CN there are, broadly speaking, two approaches to delusion. The first uses a one-stage model, in which delusions are explained as rationalizations of anomalous experiences via reasoning strategies that are not, in themselves, abnormal. Two-stage models invoke additional hypotheses about abnormalities of reasoning. In this paper, I examine what appears to be a very strong argument, developed within CN, in favor of a two-stage explanation of the difference in content between the Capgras and Cotard delusions. That explanation treats them as alternative rationalizations of essentially the same phenomenology. I show, however, that once we distinguish the phenomenology (and the neuroetiology), a one-stage model is adequate. In the final section I make some more general remarks on the one- and two-stage models.

Refining the Explanation of Cotard’s Delusion

Recent work in cognitive neuropsychiatry explains the Capgras and Cotard delusions as alternative explanations of unusual qualitative states caused by dam-age to an affective component of the face recognition system. The difference between the delusions results from differences in attributional style. Cotard patients typically exhibit a style of internal attribution associated with depression, while Capgras patients exhibit the external attribution style more typical of paranoia. Thus the Cotard patient attributes her condition to drastic changes in herself and the Capgras patient attributes the same changes to alterations in the environment. I suggest three modifications to this explanation. Firstly, the nature of the affective deficit in Cotard cases may be more global than in Capgras cases, resulting from the diffuse effects of the neurochemical substrate of depression. Secondly, this explanation gives us additional insight into the content of the delusion. It is unsurprising that persons whose global affective responses were suppressed would explain their lack of response by saying that they had no bodily existence. Finally I suggest that in Cotard cases the delusion is produced by a reasoning deficit, rather than attributional style.

The theory of mind module in evolutionary psychology

Evolutionary Psychology is based on the idea that the mind is a set of special purpose thinking devices or modules whose domain-specific structure is an adaptation to ancestral environments. The modular view of the mind is an uncontroversial description of the periphery of the mind, the input-output sensorimotor and affective subsystems. The novelty of EP is the claim that higher order cognitive processes also exhibit a modular structure. Autism is a primary case study here, interpreted as a developmental failure of a module devoted to social intelligence or Theory of Mind. In this article I reappraise the arguments for innate modularity of TOM and argue that they fail. TOM ability is a consequence of domain general development scaffolded by early, innately specified, sensorimotor abilities. The alleged Modularity of TOM results from interpreting the outcome of developmental failures characteristic of autism at too high a level of cognitive abstraction.

Delusions as performance failures

Delusions are explanations of anomalous experiences. A theory of delusion requires an explanation of both the anomalous experience and the apparently irrational explanation generated by the delusional subject. Hence, we require a model of rational belief formation against which the belief formation of delusional subjects can be evaluated. Method. I first describe such a model, distinguishing procedural from pragmatic rationality. Procedural rationality is the use of rules or procedures, deductive or inductive, that produce an inferentially coherent set of propositions. Pragmatic rationality is the use of procedural rationality in context. I then apply the distinction to the explanation of the Capgras and the Cotard delusions. I then argue that delusions are failures of pragmatic rationality. I examine the nature of these failures employing the distinction between performance and competence familiar from Chomskian linguistics. Results. This approach to the irrationality of delusions reconciles accounts in which the explanation of the anomalous experience exhausts the explanation of delusion, accounts that appeal to further deficits within the reasoning processes of delusional subjects, and accounts that argue that delusions are not beliefs at all. (Respectively, one-stage, two-stage, and expressive accounts.) Conclusion. In paradigm cases that concern cognitive neuropsychiatry the irrationality of delusional subjects should be thought of as a performance deficit in pragmatic rationality.

Does the normal brain have a theory of mind

Apperly, Samson and Humphreys [1] have elegantly detailed the empirical standards necessary to claim that theory of mind (ToM) is domain-specific. They argue convincingly that current evidence from research with neurological patients under-determines domain-specific claims, but do not describe the alternative to the domain-specific view. We sketch an explicit alternative, describing computational architecture that could support ToM inferences without requiring a specific ToM module. We argue that this view integrates evidence from both autism and neuropsychology more convincingly than the modular view.

Tacit knowledge, rule following and Pierre Bourdieu’s philosophy of social science:

Pierre Bourdieu has developed a philosophy of social science, grounded in the phenomenological tradition, which treats knowledge as a practical ability embodied in skilful behaviour, rather than an intellectual capacity for the representation and manipulation of propositional knowledge. He invokes Wittgenstein’s remarks on rule-following as one way of explicating the idea that knowledge is a skill. Bourdieu’s conception of tacit knowledge is a dispositional one, adopted to avoid a perceived dilemma for methodological individualism. That dilemma requires either the explanation of regularities in social behaviour as the result of the tacit representation of procedural rules (‘legalism’) or the self-conscious representation of behavioural goals (‘voluntarism’) by individuals. After explaining the apparent dilemma, I then argue that Wittgenstein’s remarks on rule following actually undermine, rather than support, a dispositional solution. Nonetheless, the philosophy of social science can survive without a dispositional account of knowledge. Such a social science needs, firstly, to embrace one horn of the dilemma, voluntarism, provided that the relevant regularities can be explained as unintended consequences of agents’ self-represented intentions. Secondly, such a social science should treat theorists’ interpretations as unifying generalizations, not hypotheses about the acquisition of tacit knowledge. Finally, where appeal to cognitive psychology can distinguish otherwise equivalent theories in social science, social science should incorporate the data of cognitive psychology concerning tacit mental processes.

Generous or parsimonious cognitive architecture? Cognitive neuroscience and Theory of Mind

Recent work in cognitive neuroscience on the childs Theory of Mind (ToM) has pursued the idea that the ability to metarepresent mental states depends on a domain-specific cognitive subystem implemented in specific neural circuitry: a Theory of Mind Module. We argue that the interaction of several domain-general mechanisms and lower-level domain-specific mechanisms accounts for the flexibility and sophistication of behavior, which has been taken to be evidence for a domain-specific ToM module. This finding is of more general interest since it suggests a parsimonious cognitive architecture can account for apparent domain specificity. We argue for such an architecture in two stages. First, on conceptual grounds, contrasting the case of language with ToM, and second, by showing that recent evidence in the form of fMRI and lesion studies supports the 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 Theory of Mind, Metarepresentation, and Modularity Developmental Components of ToM The Analogy with Modularity of Language Dissociations without Modules The Evidence from Neuroscience Conclusion

Nativism and Neuroconstructivism in the Explanation of Williams Syndrome

Nativists about syntactic processing have argued that linguisticprocessing, understood as the implementation of a rule-basedcomputational architecture, is spared in Williams syndrome, (WMS)subjects – and hence that it provides evidence for a geneticallyspecified language module. This argument is bolstered by treatingSpecific Language Impairments (SLI) and WMS as a developmental doubledissociation which identifies a syntax module. Neuroconstructivists haveargued that the cognitive deficits of a developmental disorder cannot beadequately distinguished using the standard gross behavioural tests ofneuropsychology and that the linguistic abilities of the WMS subject canbe equally well explained by a constructivist strategy of neurallearning in the individual, with linguisitic functions implemented in anassociationist architecture. The neuroconstructivist interpretation ofWMS undermines the hypothesis of a double dissociation between SLI andWMS, leaving unresolved the question of nativism about syntax. Theapparent linguistic virtuosity of WMS subjects is an artefact ofenhanced phonological processing, a fact which is easier to demonstratevia the associationist computational model embraced byneuroconstructivism.

Mental time travel, somatic markers and “myopia for the future”

Patients with damage to the ventromedial prefrontal cortex (VMPFC) are often described as having impaired ability for planning and decision making despite retaining intact capacities for explicit reasoning. The somatic marker hypothesis is that the VMPFC associates implicitly represented affective information with explicit representations of actions or outcomes. Consequently, when the VMPFC is damaged explicit reasoning is no longer scaffolded by affective information, leading to characteristic deficits. These deficits are exemplified in performance on the Iowa Gambling Task (IGT) in which subjects with VMPFC perform significantly worse than neurotypicals in a task which requires them learn from rewarding and punishing experience to make decisions. The somatic marker theory adopts a canonical theory of emotion, in which emotions function as part of a valencing system, to explain the role of affective processes. The first part of the paper argues against this canonical account. The second part provides a different account of the role of the role of the VMPFC in decision-making which does not depend on the canonical account of emotion. Together the first and second parts of the paper provide the basis for a different interpretation of results on the Iowa Gambling Task (IGT). In fact the IGT may be probing a deficit in what has been called mental time travel: the ability to access and use information from previous experience and imaginatively rehearse future experiences as part of the process of deliberation.