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

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

What can developmental disorders tell us about the neurocomputational constraints that shape development? the case of Williams syndrome

The uneven cognitive phenotype in the adult outcome of Williams syndrome has led some researchers to make strong claims about the modularity of the brain and the purported genetically determined, innate specification of cognitive modules. Such arguments have particularly been marshaled with respect to language. We challenge this direct generalization from adult phenotypic outcomes to genetic specification and consider instead how genetic disorders provide clues to the constraints on plasticity that shape the outcome of development. We specifically examine behavioral studies, brain imaging, and computational modeling of language in Williams syndrome but contend that our theoretical arguments apply equally to other cognitive domains and other developmental disorders. While acknowledging that selective deficits in normal adult patients might justify claims about cognitive modularity, we question whether similar, seemingly selective deficits found in genetic disorders can be used to argue that such cognitive modules are prespecified in infant brains. Cognitive modules are, in our view, the outcome of development, not its starting point. We note that most work on genetic disorders ignores one vital factor, the actual process of ontogenetic development, and argue that it is vital to view genetic disorders as proceeding under different neurocomputational constraints, not as demonstrations of static modularity

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

An alternative to domain-general or domain-specific frameworks for theorizing about human evolution and ontogenesis

This paper maintains that neither a domain-general nor a domain-specific framework is appropriate for furthering our understanding of human evolution and ontogenesis. Rather, as we learn increasingly more about the dynamics of gene-environment interaction and gene expression, theorists should consider a third alternative: a domain-relevant approach, which argues that the infant brain comes equipped with biases that are relevant to, but not initially specific to, processing different kinds of input. The hypothesis developed here is that domain-specific core knowledge/specialized functions do not constitute the start state; rather, functional specialization emerges progressively through neuronal competition over developmental time. Thus, the existence of category-specific deficits in brain-damaged adults cannot be used to bolster claims that category-specific or domain-specific modules underpin early development, because neural specificity in the adult brain is likely to have been the emergent property over time of a developing, self-structuring system in interaction with the environment

More about the same: children's understanding of post-articles

An experiment on children between 2; 0 and 7; 0 showed that they initially interpret the same X to mean ‘same kind' in contexts where it actually means ‘same one'. This led to a critical evaluation of Piaget's implicit contention that young children are using determiners anaphorically. Stress is placed on the linguistic rather than conceptual component of children's behaviour in experiments involving questions of the type: Is it the same X? It is argued that language is not only the tool of intelligence for representing ongoing cognitive development, but that it is also a problem area for children within its own right. It is suggested that the importance of young children's processing procedures on the linguistic environment has hitherto been underestimated in Piaget's interactive epistemolog

A cross-syndrome comparison of sleep-dependent learning on a cognitive procedural task

Sleep plays a key role in the consolidation of newly acquired information and skills into long term memory. Children with Down syndrome (DS) and Williams syndrome (WS) frequently experience sleep problems, abnormal sleep architecture and difficulties with learning; thus, we predicted that children from these clinical populations would demonstrate impairments in sleep-dependent memory consolidation relative to children with typical development (TD) on a cognitive procedural task: The Tower of Hanoi. Children with DS (n = 17), WS (n = 22) and TD (n = 34) completed the Tower of Hanoi task. They were trained on the task either in the morning or evening, then completed it again following counterbalanced retention intervals of daytime wake and night time sleep. Children with TD and with WS benefitted from sleep for enhanced memory consolidation and improved their performance on the task by reducing the number of moves taken to completion, and by making fewer rule violations. We did not find any large effects of sleep on learning in children with DS, suggesting that these children are not only delayed, but atypical in their learning strategies. Importantly, our findings have implications for educational strategies for all children, specifically considering circadian influences on new learning and the role of children’s night time sleep as an aid to learning.<br/

On the adaptive advantage of always being right (even when one is not)

We propose another positive illusion – overconfidence in the generalisability of one’s theory – that fits with McKay & Dennett’s (M&D’s) criteria for adaptive misbeliefs. This illusion is pervasive in adult reasoning but we focus on its prevalence in children’s developing theories. It is a strongly held conviction arising from normal functioning of the doxastic system that confers adaptive advantage on the individual