Precis of neuroconstructivism: how the brain constructs cognition

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

A visual conflict hypothesis for global-local visual deficits in Williams Syndrome: simulations and data

Individuals with Williams Syndrome demonstrate impairments in visuospatial cognition. This has been ascribed to a local processing bias. More specifically, it has been proposed that the deficit arises from a problem in disengaging attention from local features. We present preliminary data from an integrated empirical and computational exploration of this phenomenon. Using a connectionist model, we first clarify and formalize the proposal that visuospatial deficits arise from an inability to locally disengage. We then introduce two empirical studies using Navon-style stimuli. The first explored sensitivity to local vs. global features in a perception task, evaluating the effect of a manipulation that raised the salience of global organization. Thirteen children with WS exhibited the same sensitivity to this manipulation as CA-matched controls, suggesting no local bias in perception. The second study focused on image reproduction and demonstrated that in contrast to controls, the children with WS were distracted in their drawings by having the target in front of them rather than drawing from memory. We discuss the results in terms of an inability to disengage during the planning stage of reproduction due to over-focusing on local elements of the current visual stimulus

Environmental and genetic influences on neurocognitive development: the importance of multiple methodologies and time-dependent intervention

Genetic mutations and environmental factors dynamically influence gene expression and developmental trajectories at the neural, cognitive, and behavioral levels. The examples in this article cover different periods of neurocognitive development—early childhood, adolescence, and adulthood—and focus on studies in which researchers have used a variety of methodologies to illustrate the early effects of socioeconomic status and stress on brain function, as well as how allelic differences explain why some individuals respond to intervention and others do not. These studies highlight how similar behaviors can be driven by different underlying neural processes and show how a neurocomputational model of early development can account for neurodevelopmental syndromes, such as autism spectrum disorders, with novel implications for intervention. Finally, these studies illustrate the importance of the timing of environmental and genetic factors on development, consistent with our view that phenotypes are emergent, not predetermined

Models of atypical development must also be models of normal development

Functional magnetic resonance imaging studies of developmental disorders and normal cognition that include children are becoming increasingly common and represent part of a newly expanding field of developmental cognitive neuroscience. These studies have illustrated the importance of the process of development in understanding brain mechanisms underlying cognition and including children ill the study of the etiology of developmental disorders

Are developmental disorders like cases of adult brain damage? Implications from connectionist modelling

It is often assumed that similar domain-specific behavioural impairments found in cases of adult brain damage and developmental disorders correspond to similar underlying causes, and can serve as convergent evidence for the modular structure of the normal adult cognitive system. We argue that this correspondence is contingent on an unsupported assumption that atypical development can produce selective deficits while the rest of the system develops normally (Residual Normality), and that this assumption tends to bias data collection in the field. Based on a review of connectionist models of acquired and developmental disorders in the domains of reading and past tense, as well as on new simulations, we explore the computational viability of Residual Normality and the potential role of development in producing behavioural deficits. Simulations demonstrate that damage to a developmental model can produce very different effects depending on whether it occurs prior to or following the training process. Because developmental disorders typically involve damage prior to learning, we conclude that the developmental process is a key component of the explanation of endstate impairments in such disorders. Further simulations demonstrate that in simple connectionist learning systems, the assumption of Residual Normality is undermined by processes of compensation or alteration elsewhere in the system. We outline the precise computational conditions required for Residual Normality to hold in development, and suggest that in many cases it is an unlikely hypothesis. We conclude that in developmental disorders, inferences from behavioural deficits to underlying structure crucially depend on developmental conditions, and that the process of ontogenetic development cannot be ignored in constructing models of developmental disorders

Developmental disorders

Introduction: Connectionist models have recently provided a concrete computational platform from which to explore how different initial constraints in the cognitive system can interact with an environment to generate the behaviors we find in normal development (Elman et al., 1996; Mareschal & Thomas, 2000). In this sense, networks embody several principles inherent to Piagetian theory, the major developmental theory of the twentieth century. By extension, these models provide the opportunity to explore how shifts in these initial constraints (or boundary conditions) can result in the emergence of the abnormal behaviors we find in atypical development. Although this field is very new, connectionist models have already been put forward to explain disordered language development in Specific Language Impairment (Hoeffner & McClelland, 1993), Williams Syndrome (Thomas & Karmiloff-Smith, 1999), and developmental dyslexia (Seidenberg and colleagues, see e.g. Harm & Seidenberg, in press); to explain unusual characteristics of perceptual discrimination in autism (Cohen, 1994; Gustafsson, 1997); and to explore the emergence of disordered cortical feature maps using a neurobiologically constrained model (Oliver, Johnson, Karmiloff-Smith, & Pennington, in press). In this entry, we will examine the types of initial constraints that connectionist modelers typically build in to their models, and how variations in these constraints have been proposed as possible accounts of the causes of particular developmental disorders. In particular, we will examine the claim that these constraints are candidates for what will constitute innate knowledge. First, however, we need to consider a current debate concerning whether developmental disorders are a useful tool to explore the (possibly innate) structure of the normal cognitive system. We will find that connectionist approaches are much more consistent with one side of this debate than the other

Can developmental disorders be used to bolster claims from evolutionary psychology? a neuroconstructivist approach

Book synopsis: Based on the Annual Symposium of the Jean Piaget Society, Biology and Knowledge Revisited focuses on the classic issue of the relationship between nature and nurture in cognitive and linguistic development, and their neurological substrates

Colateralization of Broca's area and the visual word form area in left-handers: fMRI evidence

A

From early markers to neuro-developmental mechanisms of autism

A fast growing field, the study of infants at risk because of having an older sibling with autism (i.e. infant sibs) aims to identify the earliest signs of this disorder, which would allow for earlier diagnosis and intervention. More importantly, we argue, these studies offer the opportunity to validate existing neuro-developmental models of autism against experimental evidence. Although autism is mainly seen as a disorder of social interaction and communication, emerging early markers do not exclusively reflect impairments of the “social brain”. Evidence for atypical development of sensory and attentional systems highlight the need to move away from localized deficits to models suggesting brain-wide involvement in autism pathology. We discuss the implications infant sibs findings have for future work into the biology of autism and the development of interventions