The theory of mind (ToM) deficit associated with autism spectrum disorder has been a central topic in the debate about the modularity of the mind. In a series of papers, Philip Gerrans and Valerie Stone argue that positing a ToM module does not best explain the deficits exhibited by individuals with autism (Gerrans 2002; Stone & Gerrans 2006a, 2006b; Gerrans & Stone 2008). In this paper, I first criticize Gerrans and Stone’s (2008) account. Second, I discuss various studies of individuals (...) with autism and argue that they are best explained by positing a higher-level, domain-specific ToM module. (shrink)

The study of genetic developmental disorders originally seemed to hold the promise for those of a nativist persuasion of demonstrating pure dissociations between different cognitive functions, as well as the existence of innately specified modules in the brain and the direct mapping of mutated genes to specific cognitive-level outcomes. However, more recent research within a neuroconstructivist perspective has challenged this promise, arguing that earlier researchers lost sight of one fundamental explanatory factor in both the typical and atypical case: the actual (...) process of ontogenetic development. The paper is divided into three parts on evolution, genetics, and ontogeny. Each section starts by examining nativist claims about innateness and modularity of function, and subsequently evaluates them within a neuroconstructivist approach to human development. (shrink)

We show how an epistemology informed by cognitive science promises to shed light on an ancient problem in the philosophy of mathematics: the problem of exactness. The problem of exactness arises because geometrical knowledge is thought to concern perfect geometrical forms, whereas the embodiment of such forms in the natural world may be imperfect. There thus arises an apparent mismatch between mathematical concepts and physical reality. We propose that the problem can be solved by emphasizing the ways in which the (...) brain can transform and organize its perceptual intake. It is not necessary for a geometrical form to be perfectly instantiated in order for perception of such a form to be the basis of a geometrical concept. (shrink)

N-methyl-d-aspartate receptor (NMDAR) dysfunction plays a crucial role in schizophrenia, leading to impairments in cognitive coordination. NMDAR agonists (e.g., glycine) ameliorate negative and cognitive symptoms, consistent with NMDAR models. However, not all types of cognitive coordination use NMDAR. Further, not all aspects of cognitive coordination are impaired in schizophrenia, suggesting the need for specificity in applying the cognitive coordination construct.

To understand schizophrenia, a linking hypothesis is needed that shows how brain mechanisms lead to behavioral functions in normals, and also how breakdowns in these mechanisms lead to behavioral symptoms of schizophrenia. Such a linking hypothesis is now available that complements the discussion offered by Phillips & Silverstein (P&S).

Theories of children's developing understanding of mind tend to emphasize either individualistic processes of theory formation, maturation, or introspection, or the process of enculturation. However, such theories must be able to account for the accumulating evidence of the role of social interaction in the development of social understanding. We propose an alternative account, according to which the development of children's social understanding occurs within triadic interaction involving the child's experience of the world as well as communicative interaction with others about (...) their experience and beliefs (Chapman 1991; 1999). It is through such triadic interaction that children gradually construct knowledge of the world as well as knowledge of other people. We contend that the extent and nature of the social interaction children experience will influence the development of children's social understanding. Increased opportunity to engage in cooperative social interaction and exposure to talk about mental states should facilitate the development of social understanding. We review evidence suggesting that children's understanding of mind develops gradually in the context of social interaction. Therefore, we need a theory of development in this area that accords a fundamental role to social interaction, yet does not assume that children simply adopt socially available knowledge but rather that children construct an understanding of mind within social interaction. Key Words: language; Piaget; social interaction; theories of mind; Vygotsky; Wittgenstein. (shrink)

Phillips & Silverstein argue that a range of cognitive disturbances in schizophrenia result from a deficit in cognitive coordination attributable to NMDA receptor dysfunction. We suggest that the viability of this hypothesis would be further supported by explicit implementation in a computational framework that can produce quantitative estimates of the behavior of both healthy individuals and individuals with schizophrenia.

In his novel Remembrance of Things Past, Marcel Proust argues that conventional descriptions of the phenomenology of consciousness are incomplete because they focus too much on the highly-salient sensory information that dominates each moment of awareness and ignore the network of associations that lies in the background. In this paper, I explicate Proust’s theory of conscious experience and show how it leads him directly to a theory of aesthetic perception. Proust’s division of awareness into two components roughly corresponds to William (...) James’ division of the stream of thought into a “nucleus” and “fringe.” Proust argues that the function of art is to evoke the underlying associative network indirectly in the mind of the observer by using carefully chosen sensory surfaces to control the stream of thought. I propose a possible neural basis for this Proustian/Jamesian phenomenology, and argue that the general principles of Proustian aesthetics can be applied to all forms of art. I conclude that a scientific theory of art should follow in a straightforward manner from a scientific theory of consciousness. (shrink)

The broad issue in this paper is the relationship between cognitive psychology and neuroscience. That issue arises particularly sharply for cognitive neurospsychology, some of whose practitioners claim a methodological autonomy for their discipline. They hold that behavioural data from neuropsychological impairments are sufficient to justify assumptions about the underlying modular structure of human cognitive architecture, as well as to make inferences about its various components. But this claim to methodological autonomy can be challenged on both philosophical and empirical grounds. A (...) priori considerations about (cognitive) multiple realisability challenge the thesis on philosophical grounds, and neuroscientific findings from developmental disorders substantiate that challenge empirically. The conclusion is that behavioural evidence alone is inadequate for scientific progress since appearances of modularity can be thoroughly deceptive, obscuring both the dynamic processes of neural development and the endstate network architecture of real cognitive systems. (shrink)

How should we go about developing emotion taxonomies suitable for a science of emotion? Scientific categories are supposed to be “projectable”: They must support generalizations required for the scientific practices of induction and explanation. Attempts to provide projectable emotion categories typically classify emotions in terms of a limited set of modules, but such taxonomies have had limited uptake because they arguably misrepresent the diversity of our emotional repertoire. However, more inclusive, non-modular, taxonomies also prove problematic, for they struggle to meet (...) the projectability constraint. In this paper, I explain how a developmental approach to emotion, one that utilizes the notion of progressive modularization, can help us approach emotion categorization in a more inclusive and projectable manner. (shrink)

Theory of illness causation is an important issue in all biomedical sciences, and solid etiological explanations are needed in order to develop therapeutic approaches in medicine and preventive interventions in public health. Until now, the literature about the theoretical underpinnings of illness causation research has been scarce and fragmented, and lacking a convenient summary. This interdisciplinary book provides a convenient and accessible distillation of the current status of research into this developing field, and adds a personal flavor to the discussion (...) by proposing the etiological stance as a comprehensive approach to identify modifiable causes of illness. (shrink)

The Darwinian theory of evolution is itself evolving and this book presents the details of the core of modern Darwinism and its latest developmental directions. The authors present current scientific work addressing theoretical problems and challenges in four sections, beginning with the concepts of evolution theory, its processes of variation, heredity, selection, adaptation and function, and its patterns of character, species, descent and life. The second part of this book scrutinizes Darwinism in the philosophy of science and its usefulness in (...) understanding ecosystems, whilst the third section deals with its application in disciplines beyond the biological sciences, including evolutionary psychology and evolutionary economics, Darwinian morality and phylolinguistics. The final section addresses anti-Darwinism, the creationist view and issues around teaching evolution in secondary schools. The reader learns how current experimental biology is opening important perspectives on the sources of variation, and thus of the very power of natural selection. This work examines numerous examples of the extension of the principle of natural selection and provides the opportunity to critically reflect on a rich theory, on the methodological rigour that presides in its extensions and exportations, and on the necessity to measure its advantages and also its limits. Scholars interested in modern Darwinism and scientific research, its concepts, research programs and controversies will find this book an excellent read, and those considering how Darwinism might evolve, how it can apply to the human sciences and other disciplines beyond its origins will find it particularly valuable. Originally produced in French (Les Mondes Darwiniens), the scope and usefulness of the book have led to the production of this English text, to reach a wider audience. This book is a milestone in the impressive penetration by Francophone scholars into the world of Darwinian science, its historiography and philosophy over the last two decades. Alex Rosenberg, R. Taylor Cole Professor of Philosophy, Duke University Until now this useful and comprehensive handbook has only been available to francophones. Thanks to this invaluable new translation, this collection of insightful and original essays can reach the global audience it deserves. Tim Lewens, University of Cambridge. (shrink)

Language evolution resulted from changes in our biology, behavior, and culture. One source of these changes might be human self-domestication. Williams syndrome (WS) is a clinical condition with a clearly defined genetic basis and resulting in a distinctive behavioral and cognitive profile, including enhanced sociability. In this paper we show evidence that the WS phenotype can be satisfactorily construed as a hyper-domesticated human phenotype, plausibly resulting from the effect of the WS hemydeletion on selected candidates for domestication and neural crest (...) function. Specifically, we show that genes involved in animal domestication and neural crest development and function are significantly dysregulated in the blood of subjects with WS. We also discuss the consequences of this link between domestication and WS for our current understanding of language evolution. (shrink)

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. (shrink)

In the multidisciplinary field of developmental cognitive neuroscience, statistical associations between levels of description play an increasingly important role. One example of such associations is the observation of correlations between relatively common gene variants and individual differences in behavior. It is perhaps surprising that such associations can be detected despite the remoteness of these levels of description, and the fact that behavior is the outcome of an extended developmental process involving interaction of the whole organism with a variable environment. Given (...) that they have been detected, how do such associations inform cognitive-level theories? To investigate this question, we employed a multiscale computational model of development, using a sample domain drawn from the field of language acquisition. The model comprised an artificial neural network model of past-tense acquisition trained using the backpropagation learning algorithm, extended to incorporate population modeling and genetic algorithms. It included five levels of description—four internal: genetic, network, neurocomputation, behavior; and one external: environment. Since the mechanistic assumptions of the model were known and its operation was relatively transparent, we could evaluate whether cross-level associations gave an accurate picture of causal processes. We established that associations could be detected between artificial genes and behavioral variation, even under polygenic assumptions of a many-to-one relationship between genes and neurocomputational parameters, and when an experience-dependent developmental process interceded between the action of genes and the emergence of behavior. We evaluated these associations with respect to their specificity, to their developmental stability, and to their replicability, as well as considering issues of missing heritability and gene–environment interactions. We argue that gene–behavior associations can inform cognitive theory with respect to effect size, specificity, and timing. The model demonstrates a means by which researchers can undertake multiscale modeling with respect to cognition and develop highly specific and complex hypotheses across multiple levels of description. (shrink)

Phillips & Silverstein offer an exciting synthesis of ongoing efforts to link the clinical and cognitive manifestations of schizophrenia with cellular accounts of its pathophysiology. We applaud their efforts but wonder whether the highly inclusive notion of “context” adequately captures some important details regarding schizophrenia and NMDA/glutamate function that are suggested by work on language processing and cognitive electrophysiology.

How can we explain the intentional nature of an expert’s actions, performed without immediate and conscious control, relying instead on automatic cognitive processes? How can we account for the differences and similarities with a novice’s performance of the same actions? Can a naturalist explanation of intentional expert action be in line with a philosophical concept of intentional action? Answering these and related questions in a positive sense, this dissertation develops a three-step argument. Part I considers different methods of explanations in (...) cognitive neuroscience (Bennett & Hacker’s philosophical, conceptual analysis; Marr’s three levels of explanation; Neural Correlates of Consciousness research; mechanistic explanation), defending ‘mechanistic explanation’ as a method that provides the necessary tools for integrating interdisciplinary insights into human action. Furthermore, a dynamic, explanatory mechanism allows the assessment of the impact of learning and development on expert action in a valuable way that other methods don’t. Part II continues by scrutinizing several cognitive neuroscientific theories of learning and development (neuroconstructivism; dual-processing theories; simulation theory; extended mind/cognition hypothesis), arguing for the complex interactions between different types of processing and different action representations involved in expert action performances. Moreover, according to our discussion of a particular ‘simulation theory’ these interactions can be influenced in several ways with the use of language, allowing an agent to configure a specific action representation for performance at a later stage. The results of Parts I and II are then applied in Part III to a parallel discussion of philosophical analyses of intentional action (discussing i.a. Frankfurt, Bratman, Pacherie and Ricoeur) and cognitive neuroscientific insights in it. Both approaches are found to converge in emphasizing the importance for an expert to develop stable patterns of actions that comply maximally not only with his intentions, but also with his motor expertise and with situational conditions. Consequently, his actions – automatic, or not – rely on this ‘sculpted space of actions’. (shrink)

This article addresses the relations between ‘nature’ and ‘culture’ (and those characteristics associated with ‘the natural’ and ‘the cultural’) in the context of the debates about Prozac. Following Marilyn Strathern, I focus specifically on the contested issue of enablement - that is, on what Prozac does or does not enable, and on the relation between enablement and enhancement, normality and pathology. I argue that the implications of the model of the brain that accompanies explanations of Prozac are such that commentators (...) are obliged to address not only the nature of normality but also the nature of nature itself. Through a close analysis of these debates, I suggest that critiques of Prozac should be understood not as objections to reductionism - to a biology that closes things down - but rather to one that opens things up: that opens up the relations between nature, culture, biology and the individual, relations that are now cross-cut and thrown about by artificiality. Objections to Prozac, then, might be characterized as an attempt to put these concepts back into their ‘proper’ positions, to re-establish the relationality between them. In conclusion, I argue that the biology put forward by proponents of psychopharmacology, regardless of the desirability of the latter, challenges not only the frequent assumptions that are made about the claims of materialist science, but also some of the terms and concepts that are commonly deployed in the social sciences. (shrink)

The compelling case that Anderson makes for neural reuse and against modularity as organizing principle of the brain is further supported by evidence from developmental disorders. However, to provide a full evolutionary-developmental theory of neural reuse that encompasses both typical and atypical development, Anderson's (MRH) could be further constrained by considering brain development across ontogeny.

The pivotal problem of comorbidity research lies in the psychometric foundation it rests on, that is, latent variable theory, in which a mental disorder is viewed as a latent variable that causes a constellation of symptoms. From this perspective, comorbidity is a (bi)directional relationship between multiple latent variables. We argue that such a latent variable perspective encounters serious problems in the study of comorbidity, and offer a radically different conceptualization in terms of a network approach, where comorbidity is hypothesized to (...) arise from direct relations between symptoms of multiple disorders. We propose a method to visualize comorbidity networks and, based on an empirical network for major depression and generalized anxiety, we argue that this approach generates realistic hypotheses about pathways to comorbidity, overlapping symptoms, and diagnostic boundaries, that are not naturally accommodated by latent variable models: Some pathways to comorbidity through the symptom space are more likely than others; those pathways generally have the same direction (i.e., from symptoms of one disorder to symptoms of the other); overlapping symptoms play an important role in comorbidity; and boundaries between diagnostic categories are necessarily fuzzy. (shrink)

In chronic schizophrenic patients with both positive and negative symptoms (see Table 1), interhemispheric connections at the high frequency beta2-rhythm are absent during cognitive tasks, in contrast to normal controls, who have many interhemispheric connections at this frequency in the same situation. Connectivity is a fundamental brain feature, evidently greatly promoted by the NMDA system. It is a more reliable measure of brain function than the spectral power of this rhythm.

Neuroconstructivism: How the Brain Constructs Cognition proposes a unifying framework for the study of cognitive development that brings together (1) constructivism (which views development as the progressive elaboration of increasingly complex structures), (2) cognitive neuroscience (which aims to understand the neural mechanisms underlying behavior), and (3) computational modeling (which proposes formal and explicit specifications of information processing). The guiding principle of our approach is context dependence, within and (in contrast to Marr [1982]) between levels of organization. We propose that three (...) mechanisms guide the emergence of representations: competition, cooperation, and chronotopy; which themselves allow for two central processes: proactivity and progressive specialization. We suggest that the main outcome of development is partial representations, distributed across distinct functional circuits. This framework is derived by examining development at the level of single neurons, brain systems, and whole organisms. We use the terms encellment, embrainment, and embodiment to describe the higher-level contextual influences that act at each of these levels of organization. To illustrate these mechanisms in operation we provide case studies in early visual perception, infant habituation, phonological development, and object representations in infancy. Three further case studies are concerned with interactions between levels of explanation: social development, atypical development and within that, developmental dyslexia. We conclude that cognitive development arises from a dynamic, contextual change in embodied neural structures leading to partial representations across multiple brain regions and timescales, in response to proactively specified physical and social environment. (shrink)

Impairments in cognitive coordination in schizophrenia are supported by phenomenological data that suggest deficits in the processing of visual context. Although the target article is sympathetic to such a phenomenological perspective, we argue that the relevance of phenomenological data for a wider understanding of consciousness in schizophrenia is not sufficiently addressed by the authors.

Numerous searches have failed to identify a single co-occurrence of total blindness and schizophrenia. Evidence that blindness causes loss of certain NMDA-receptor functions is balanced by reports of compensatory gains. Connections between visual and anterior cingulate NMDA-receptor systems may help to explain how blindness could protect against schizophrenia.

The concept of locally specialized functions dominates research on higher brain function and its disorders. Locally specialized functions must be complemented by processes that coordinate those functions, however, and impairment of coordinating processes may be central to some psychotic conditions. Evidence for processes that coordinate activity is provided by neurobiological and psychological studies of contextual disambiguation and dynamic grouping. Mechanisms by which this important class of cognitive functions could be achieved include those long-range connections within and between cortical regions that (...) activate synaptic channels via NMDA-receptors, and which control gain through their voltage-dependent mode of operation. An impairment of these mechanisms is central to PCP-psychosis, and the cognitive capabilities that they could provide are impaired in some forms of schizophrenia. We conclude that impaired cognitive coordination due to reduced ion flow through NMDA-channels is involved in schizophrenia, and we suggest that it may also be involved in other disorders. This perspective suggests several ways in which further research could enhance our understanding of cognitive coordination, its neural basis, and its relevance to psychopathology. Key Words: attention; cerebral cortex; cognitive coordination; cognitive neuropsychiatry; cognitive neuropsychology; context disorganization; Gamma rhythms; Gestalt theory; glutamate; grouping; memory; NMDA-receptors; PCP-psychosis; perceptual organization; schizophrenia. (shrink)

This commentary challenges the authors to use their computational modeling techniques to support one of their central claims: that schizophrenic deficits in bottom-up (Gestalt-type tasks) and top-down (cognitive control tasks) context processing tasks arise from the same dysfunction. Further clarification about the limits of cognitive coordination would also strengthen the hypothesis.

Neurophysiological investigations of the past two decades have consistently demonstrated a deficit in sensory gating associated with schizophrenia. Phillips & Silverstein interpret this impairment as being consistent with cognitive coordination dysfunction. However, the physiological mechanisms that underlie sensory gating have not been shown to involve gamma-band oscillations or NMDA-receptors, both of which are critical neural elements in the cognitive coordination model.

Modules are widely held to play a central role in explaining mental development and in accounts of the mind generally. But there is much disagreement about what modules are, which shows that we do not adequately understand modularity. This paper outlines a Fodoresque approach to understanding one type of modularity. It suggests that we can distinguish modular from nonmodular cognition by reference to the kinds of process involved, and that modular cognition differs from nonmodular forms of cognition in being a (...) special kind of computational process. The paper concludes by considering implications for the role of modules in explaining mental development. (shrink)

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. (shrink)

has a more specific role to play in the development of Of course, the conclusion to draw is not that innateness innate cognitive structure. In particular, a common claim claims are trivially false or that they cannot be character-.

This chapter discusses what is the specific difference of mental function, relative to the general concept of a biological function. It contrasts various approaches of this problem through evolutionary psychology, developmental system theory and neuroscientific growth theory models. It concludes that an holistic, dynamic approach to mental function suggests to reject the traditional division in mental faculties.

What was the role of music in the evolutionary history of human beings? We address this question from the point of view that musicality can be defined as a cognitive trait. Although it has been argued that we will never know how cognitive traits evolved (Lewontin, 1998), we argue that we may know the evolution of music by investigating the fundamental cognitive mechanisms of musicality, for example, relative pitch, tonal encoding of pitch, and beat induction. In addition, we show that (...) a nomological network of evidence (Schmitt & Pilcher, 2004) can be built around the hypothesis that musicality is a cognitive adaptation. Within this network, different modes of evidence are gathered to support a specific evolutionary hypothesis. We show that the combination of psychological, medical, physiological, genetic, phylogenetic, hunter–gatherer, and cross-cultural evidence indicates that musicality is a cognitive adaptation. (shrink)

The theory of mind (ToM) deficit associated with autism has been a central topic in the debate about the modularity of the mind. Most involved in the debate about the explanation of the ToM deficit have failed to notice that autism’s status as a spectrum disorder has implications about which explanation is more plausible. In this paper, I argue that the shift from viewing autism as a unified syndrome to a spectrum disorder increases the plausibility of the explanation of the (...) ToM deficit that appeals to a domain-specific, higher-level ToM module. First, I discuss what it means to consider autism as a spectrum rather than as a unified disorder. Second, I argue for the plausibility of the modular explanation on the basis that autism is better considered as a spectrum disorder. Third, I respond to a potential challenge to my account from Philip Gerrans and Valerie Stone’s recent work (Gerrans, Biol Philos 17:305–321, 2002; Stone and Gerrans, Trends Cogn Sci 10:3–4, 2006a; Soc Neurosci 1:309–319, 2006b; Gerrans and Stone, Br J Philos Sci 59:121–141, 2008). (shrink)

Phillips & Silverstein's focus on schizophrenia as a failure of “cognitive coordination” is welcome. They note that a simple hypothesis of reduced Gamma synchronisation subserving impaired coordination does not fully account for recent observations. We suggest that schizophrenia reflects a dynamic compensation to a core deficit of coordination, expressed either as hyper- or hyposynchronisation, with neurotransmitter systems and arousal as modulatory mechanisms.

Phillips & Silverstein's ambitious link between receptor abnormalities and the symptoms of schizophrenia involves a certain amount of fuzziness: No detailed mechanism is suggested through which the proposed abnormality would lead to psychological traits. We propose that detailed simulation of brain regions, using model neural networks, can aid in understanding the relation between biological abnormality and psychological dysfunction in schizophrenia.

This commentary highlights methods for using scalp EEG to make inferences about contextual field interactions, which, in view of the target article, may be specially relevant to the study of schizophrenia. Although scalp EEG has limited spatial resolution, prior knowledge combined with experimental manipulations may be used to strengthen inferences about underlying brain processes. Both spatial and temporal context are discussed within the framework of nonlinear interactions. Finally, results from a visual contour integration EEG pilot study are summarized in view (...) of a hypothesis that relates receptive field and contextual field processing to evoked and induced activity, respectively. (shrink)

This commentary addresses: (a) the problems of definition which have been prominent in the use of the term context in schizophrenia research; (b) potentially useful distinctions and links with other theories of schizophrenic cognition; and (c) possible pathways to schizophrenic symptoms. It is suggested that at least two major aspects of the operation of context may be distinguished and that both may be impaired in schizophrenia.