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

Developmental disorders of vision

This review of developmental disorders of vision focuses on a few of the many disorders that disrupt visual development. Given the enormity of the human visual system in the primate brain and complexity of visual development, however, there are likely hundreds or thousands of potential types of disorders affecting high-level vision. The rapid progress seen in developmental dyslexia and Williams syndrome demonstrates the possibilities and difficulties inherent in researching such disorders, and the authors hope that similar progress will be made for congenital prosopagnosia and other disorders in the near future

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

DNA strand break repair and neurodegeneration.

A number of DNA repair disorders are known to cause neurological problems. These disorders can be broadly characterised into early developmental, mid-to-late developmental or progressive. The exact developmental processes that are affected can influence disease pathology, with symptoms ranging from early embryonic lethality to late-onset ataxia. The category these diseases belong to depends on the frequency of lesions arising in the brain, the role of the defective repair pathway, and the nature of the mutation within the patient. Using observations from patients and transgenic mice, we discuss the importance of double strand break repair during neuroprogenitor proliferation and brain development and the repair of single stranded lesions in neuronal function and maintenance

Neurobiology of dyslexia : A reinterpretation of the data

Theories of developmental dyslexia differ on how to best interpret the great variety of symptoms (linguistic, sensory, motor) observed in dyslexic individuals. One approach views dyslexia as a specific phonological deficit, which sometimes co-occurs with a more general sensorimotor syndrome. The present review of the neurobiology of dyslexia shows that neurobiological data are indeed consistent with this view, explaining both how a specific phonological deficit might arise, and why a sensorimotor syndrome should be significantly associated with it. This new conceptualisation of the aetiology of dyslexia may generalise to other neuro-developmental disorders, and may further explain heterogeneity within each disorder and co-morbidity between 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

Language acquisition in developmental disorders

In this chapter, I review recent research into language acquisition in developmental disorders, and the light that these findings shed on the nature of language acquisition in typically developing children. Disorders considered include Specific Language Impairment, autism, Down syndrome, and Williams syndrome. I argue that disorders of language should be construed in terms of differences in the constraints that shape the learning process, rather than in terms of the normal system with components missing or malfunctioning. I outline the integrative nature of this learning process and how properties such as redundancy and compensation may be key characteristics of learning systems with atypical constraints. These ideas, as well as the new methodologies now being used to study variations in pathways of language acquisition, are illustrated with case studies from Williams syndrome and Specific Language Impairment

The role of family relationships in eating disorders in adolescents: a narrative review

Abstract: Background: Adolescents’eatingdisordershavebeenexploredthroughvariousconceptual andempiricalmodels. Onlyrecently,scientificliteratureinthisareahasmorespecificallyinvestigated theroleofrelationships,withparticularattentiontofamilyfunctioning. Objective: Thispaperreviews family relationships aspects of eating disorders in adolescence. Methods: A narrative literature review of relational issues in adolescents’ eating disorders was performed. Results: Empirical evidence of family relationships in adolescents’ eating disorders confirms the relevance of relational aspects in the development and maintenance of the pathology. In particular, the contribution of the relational-systemic approach is wide, suggesting the need to refer to the family context for a better understanding of adolescents’ sufferance. Additionally, the empirical contributions from the conceptual model of Developmental Psychopathology, highlighting the importance of risk and protection factors in family relationships, provides knowledge about the phenomenon of adolescents’ eating disorders in terms of complexity. Conclusions: An integrated relational model aimed to explore adolescents’ eating disorders is worthy of investigation to accomplish specific program of intervention