Connectionist models aiming to reveal the mechanisms of atypical development must in their undamaged form constitute plausible models of normal development and follow a developmental trajectory that matches empirical data. Constructivist models that adapt their structure to the learning task satisfy this demand. They are therefore more informative in the study of atypical development than the static models employed by Thomas & Karmiloff-Smith (T&K-S).

In this response, we consider four main issues arising from the commentaries to the target article. These include further details of the theory of interactive specialization, the relationship between neuroconstructivism and selectionism, the implications of neuroconstructivism for the notion of representation, and the role of genetics in theories of development. We conclude by stressing the importance of multidisciplinary approaches in the future study of cognitive development and by identifying the directions in which neuroconstructivism can expand in the Twenty-first Century.

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. Key Words: Acquired and developmental disorders; connectionist models; modularity; past tense; reading. (shrink)

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)

Dehaene (in Reading in the Brain) reviews and finds support for the phonological deficit hypothesis of developmental dyslexia, which proposes that dyslexics have a basic deficit in processing the constituents of spoken words. This hypothesis can be seen as reflecting three associated claims: a) there is only one basic kind of dyslexia; b) all (or most) dyslexic children have phonological impairments, and c) these phonological impairments cause their dyslexia. We consider each of these claims, and the evidence presented by Dehaene, (...) and conclude that questions remain about all three. Phonological deficits alone seem unlikely to be able to account for the complexity and heterogeneity of developmental dyslexia. (shrink)

Dehaene (in Reading in the Brain) reviews and finds support for the phonological deficit hypothesis of developmental dyslexia, which proposes that dyslexics have a basic deficit in processing the constituents of spoken words. This hypothesis can be seen as reflecting three associated claims: a) there is only one basic kind of dyslexia; b) all (or most) dyslexic children have phonological impairments, and c) these phonological impairments cause their dyslexia. We consider each of these claims, and the evidence presented by Dehaene, (...) and conclude that questions remain about all three. Phonological deficits alone seem unlikely to be able to account for the complexity and heterogeneity of developmental dyslexia. (shrink)