Attentional difficulties, both at home and in the classroom, are reported across a number of neurodevelopmental disorders. However, exactly how attention influences early socio-cognitive learning remains unclear. We addressed this question both concurrently and longitudinally in a cross-syndrome design, with respect to the communicative domain of vocabulary and to the cognitive domain of early literacy, and then extended the analysis to social behavior. Participants were young children (aged 4 to 9 years at Time 1) with either Williams syndrome (WS, N=26) (...) or Down syndrome (DS, N=26) and typically developing controls (N=103). Children with WS displayed significantly greater attentional deficits (as indexed by teacher report of behavior typical of attention deficit hyperactivity disorder, ADHD) than children with DS, but both groups had greater attentional problems than the controls. Despite their attention differences, children with DS and those with WS were equivalent in their cognitive abilities of reading single words, both at Time 1 and 12 months later, at Time 2, although they differed in their early communicative abilities in terms of vocabulary. Greater ADHD-like behaviors predicted poorer subsequent literacy for children with DS, but not for children with WS, pointing to syndrome-specific attentional constraints on specific aspects of early development. Overall, our findings highlight the need to investigate more precisely whether and, if so, how, syndrome-specific profiles of behavioral difficulties constrain learning and socio-cognitive outcomes across different domains. (shrink)
Nowadays, it is widely accepted that there is no single influence (be it nature or nurture) on cognitive development. Cognitive abilities emerge as a result of interactions between gene expression, cortical and subcortical brain networks, and environmental influences. In recent years, our study of neurodevelopmental disorders has provided much valuable information on how genes, brain development, behaviour, and environment interact to influence development from infancy to adulthood. This is the first book to present evidence on development across the lifespan across (...) these multiple levels of description (genetic, brain, cognitive, environmental). In the book, the authors have chosen a well-defined disorder, Williams syndrome (WS), to explore the impact of genes, brain development, behaviour, as well as the individual's environment on development. WS is used as a model disorder to demonstrate the authors approach to understanding development, whilst being presented in comparison to other neurodevelopmental disorders - Autism, Developmental Dyscalculia, Down syndrome, Dyslexia, Fragile X syndrome, Prader-Willi syndrome, Specific Language Impairment, Turner syndrome - to illustrate differences in development across neurodevelopmental disorders. -/- Williams syndrome is particularly informative for exploring development: Firstly, it has been extensively researched at multiple levels: genes, brain, cognition and behaviour, as well as in terms of the difficulties of daily living and social interaction. Secondly, it has been studied across the lifespan, with many studies on infants and toddlers with WS as well as a large number on children, adolescents and adults. The authors also explore a number of domain-general and domain-specific processes in the verbal, non-verbal and social domains, across numerous neurodevelopmental disorders. This illustrates, among other factors, the importance of developmental timing, i.e. that the development of a cognitive skill at a specific timepoint can impact on subsequent development within that domain, but also across domains. In addition, the authors discuss the value of investigating basic-level abilities from as close to the infant start-state as possible, presenting evidence of where cross-syndrome comparisons have shed light on the cascading impacts of subtle similarities and discrepancies in early delay or deviance, on subsequent development. -/- Designed such that readers with an interest in any neurodevelopmental disorder can gain insight into the intricate dynamics of cognitive development, the book covers both theoretical issues and those of clinical relevance. It will be an invaluable reference for any researcher, clinician, student as well as interested parents or teachers wishing to learn about neurodevelopmental disorders from a developmental framework. -/- . (shrink)
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.
The target article by Locke & Bogin (L&B) focuses on the evolution of language as a communicative tool. They neglect, however, that from infancy onwards humans have the ability to go beyond successful behaviour and to reflect upon language (and other domains of knowledge) as a problem space in its own right. This ability is not found in other species and may well be what makes humans unique.
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 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 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.
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)
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.
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.