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)
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)
In response to our target article, many of the commentators concentrated on our notion of Residual Normality. In our response, we focus on the questions raised by this idea. However, we also examine broader issues concerning the importance of incorporating a realistic theory of the process of development into explanations of developmental deficits.
In this commentary we raise three issues: (1) Is it motherese or song that sets the stage for very early mother-infant interaction? (2) Does the infant play a pivotal role in the complex temporal structure of social interaction? (3) Is the vocal channel primordial or do other modalities play an equally important role in social interaction?
In this commentary, we outline an epistemological continuum between earlier and later number concepts, showing how empirical findings support the view that specific and general underpinnings to number develop in parallel in children; and we raise the question, based on cross-syndrome comparisons in infancy, as to whether exact or approximate number abilities underlie these later skills.
We add to the constructivist approach of Quartz & Sejnowski (Q&S) by outlining a specific classification of sources of constraint on the emergence of representations from Elman et al. (1996). We suggest that it is important to consider behavioral constructivism in addition to neural constructivism.
We welcome network theory as a tool for modelling the multi-directional interactions that characterise disease. However, we feel that Cramer et al. have neglected one important aspect: how diseases change over developmental time. We discuss principles such as fan in, fan out, bottlenecks, and common pathways, and argue that modelling these developmental aspects can be vital, particularly in deriving properly targeted treatments.
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.
This commentary questions the applicability of the Newell Test for evaluating the utility of connectionism. Rather than being a specific theory of cognition (because connectionism can be used to model nativist, behaviorist, or constructivist theories), connectionism, we argue, offers researchers a collection of computational and conceptual tools that are particularly useful for investigating and rendering specific fundamental issues of human development. These benefits of connectionism are not well captured by evaluating it against Newell's criteria for a unified theory of cognition.
I respond to three continuing commentaries on Beyondmodularity, two concerning the representational redescription (RR) framework and its attempts to account for the growing flexibility of human intelligence, and one relating to the putative mysteries of developmental timing. I discuss misunderstandings about the RR framework as well as some of its shortcomings. I strongly reject the notion of a genetic clock and go on to argue for epigenetic outcomes in which genes and environment interact during the protracted period of postnatal brain (...) development. (shrink)
In this commentary, we raise two issues. First, we argue that in any species, the comparative study of metacognitive abilities must be approached from a developmental perspective and not solely from the adult end state. This makes it possible to explore the trajectories by which different species reach their phenotypic outcome and whether different cognitive systems interact over developmental time. Second, using our research comparing different genetic disorders in humans, we challenge the authors' claim that it is unparsimonious to interpret (...) the same performance in humans and animals in qualitatively different ways, because even the same overt behaviour in different groups of humans can be sustained by different underlying cognitive processes. (shrink)
This book is unique in presenting evidence on development across the lifespan across multiple levels of description . The authors use a well-defined disorder - Williams syndrome, to explore the impact of genes, brain development, behaviour, as well as the individual's environment on development.