4,254 research outputs found

    Developmental disorders

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    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

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

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    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

    Are developmental disorders like cases of adult brain damage? Implications from connectionist modelling

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    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

    Can developmental disorders be used to bolster claims from evolutionary psychology? a neuroconstructivist approach

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    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

    Audio-visual speech perception: a developmental ERP investigation

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    Being able to see a talking face confers a considerable advantage for speech perception in adulthood. However, behavioural data currently suggest that children fail to make full use of these available visual speech cues until age 8 or 9. This is particularly surprising given the potential utility of multiple informational cues during language learning. We therefore explored this at the neural level. The event-related potential (ERP) technique has been used to assess the mechanisms of audio-visual speech perception in adults, with visual cues reliably modulating auditory ERP responses to speech. Previous work has shown congruence-dependent shortening of auditory N1/P2 latency and congruence-independent attenuation of amplitude in the presence of auditory and visual speech signals, compared to auditory alone. The aim of this study was to chart the development of these well-established modulatory effects over mid-to-late childhood. Experiment 1 employed an adult sample to validate a child-friendly stimulus set and paradigm by replicating previously observed effects of N1/P2 amplitude and latency modulation by visual speech cues; it also revealed greater attenuation of component amplitude given incongruent audio-visual stimuli, pointing to a new interpretation of the amplitude modulation effect. Experiment 2 used the same paradigm to map cross-sectional developmental change in these ERP responses between 6 and 11 years of age. The effect of amplitude modulation by visual cues emerged over development, while the effect of latency modulation was stable over the child sample. These data suggest that auditory ERP modulation by visual speech represents separable underlying cognitive processes, some of which show earlier maturation than others over the course of development

    Love is . . . an abstract word: the influence of phonological and semantic factors on verbal short-term memory in Williams syndrome

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    It has been claimed that verbal short-term memory in Williams syndrome is characterised by an over-use of phonological coding alongside a reduced contribution of lexical semantics. We critically examine this hypothesis and present results from a memory span task comparing performance on concrete and abstract words, together with a replication of a span task using phonologically similar and phonologically dissimilar words. Fourteen participants with Williams syndrome were individually matched to two groups of typically developing children. The first control group was matched on digit span and the second on vocabulary level. Significant effects were found for both the semantic and the phonological variables in the WS group as well as in the control groups, with no interaction between experimental variable and group in either experiment. The results demonstrate that, despite claims to the contrary, children and adults with WS are able to access and make use of lexical semantics in a verbal short-term memory task in a manner comparable to typically developing individuals

    FGF/heparin differentially regulates Schwann cell and olfactory ensheathing cell interactions with astrocytes: a role in astrocytosis

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    After injury, the CNS undergoes an astrocyte stress response characterized by reactive astrocytosis/proliferation, boundary formation, and increased glial fibrillary acidic protein (GFAP) and chondroitin sulfate proteoglycan (CSPG) expression. Previously, we showed that in vitro astrocytes exhibit this stress response when in contact with Schwann cells but not olfactory ensheathing cells (OECs). In this study, we confirm this finding in vivo by demonstrating that astrocytes mingle with OECs but not Schwann cells after injection into normal spinal cord. We show that Schwann cell-conditioned media (SCM) induces proliferation in monocultures of astrocytes and increases CSPG expression in a fibroblast growth factor receptor 1 (FGFR1)-independent manner. However, SCM added to OEC/astrocyte cocultures induces reactive astrocytosis and boundary formation, which, although sensitive to FGFR1 inhibition, was not induced by FGF2 alone. Addition of heparin to OEC/astrocyte cultures induces boundary formation, whereas heparinase or chlorate treatment of Schwann cell/astrocyte cultures reduces it, suggesting that heparan sulfate proteoglycans (HSPGs) are modulating this activity. In vivo, FGF2 and FGFR1 immunoreactivity was increased over grafted OECs and Schwann cells compared with the surrounding tissue, and HSPG immunoreactivity is increased over reactive astrocytes bordering the Schwann cell graft. These data suggest that components of the astrocyte stress response, including boundary formation, astrocyte hypertrophy, and GFAP expression, are mediated by an FGF family member, whereas proliferation and CSPG expression are not. Furthermore, after cell transplantation, HSPGs may be important for mediating the stress response in astrocytes via FGF2. Identification of factors secreted by Schwann cells that induce this negative response in astrocytes would further our ability to manipulate the inhibitory environment induced after injury to promote regeneration

    Human Capital Decisions and Employee Satisfaction at Selected Hotels in India

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    Understanding the role of human capital is one of the key considerations in delivering and sustaining competitiveness. Managing employees in the hospitality industry is particularly a challenging task as the industry is considered to be labor intensive. High turnover and increasing employee demands are among the problems that are identified as threats to maintaining a strong competitive position. Successful hotels attempt to retain their best employees in an effort to adapt to changing environments and increased competition. Effective hotel human resource systems can produce positive outcomes, through effective employee retention strategies that focus on work force motivation, attitudes and perception. The positive implementation of these strategies can influence and create employee satisfaction. This study aims to focus on the relationship between the mediating variables of motivation, attitudes, perception and their effect on employee satisfaction. These findings are based upon an extensive survey carried out between April 2009 and June 2009 in the small mountainous state of Uttarakhand, located within the Indian sub-continent. Although the area of study is confined to the Kumaon region of Uttarakhand, the authors contend that the findings and implications can be applied to other remote developing tourist destinations in other regions

    Gallavotti-Cohen theorem, Chaotic Hypothesis and the zero-noise limit

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    The Fluctuation Relation for a stationary state, kept at constant energy by a deterministic thermostat - the Gallavotti-Cohen Theorem -- relies on the ergodic properties of the system considered. We show that when perturbed by an energy-conserving random noise, the relation follows trivially for any system at finite noise amplitude. The time needed to achieve stationarity may stay finite as the noise tends to zero, or it may diverge. In the former case the Gallavotti-Cohen result is recovered, while in the latter case, the crossover time may be computed from the action of `instanton' orbits that bridge attractors and repellors. We suggest that the `Chaotic Hypothesis' of Gallavotti can thus be reformulated as a matter of stochastic stability of the measure in trajectory space. In this form this hypothesis may be directly tested
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