The emergence of psychopathy: implications for the neuropsychological approach to developmental disorders

In this paper, I am going to examine the disorder of psychopathy and consider how genetic anomalies could give rise to the relatively specific neuro-cognitive impairments seen in individuals with this disorder. I will argue that genetic anomalies in psychopathy reduce the salience of punishment information (perhaps as a function of noradrenergic disturbance). I will argue that the ability of the amygdala to form the stimulus-punishment associations necessary for successful socialization is disrupted and that because of this, individuals with psychopathy do not learn to avoid actions that will harm others. It is noted that this model follows the neuropsychological approach to the study of developmental disorders, an approach that has been recently criticized. I will argue that these criticisms are less applicable to psychopathy. Indeed, animal work on the development of the neural systems necessary for emotion, does not support a constructivist approach with respect to affect. Importantly, such work indicates that while environmental effects can alter the responsiveness of the basic neural architecture mediating emotion, environmental effects do not construct this architecture. However, caveats to the neuropsychological approach with reference to this disorder are noted.     

Cognitive deficits in developmental disorders

The existence of specific developmental disorders such as dyslexia and autism raises interesting issues about the structure of the normally developing mind. In these disorders distinct cognitive deficits can explain a range of behavioural impairments and have the potential to be linked to specific brain abnormalities. One possibility is that there are specific mechanisms dedicated to particular types of information processing. These mechanisms may function independently of more general information processing systems and may have a distinct anatomical basis in the brain.     

Mixing qualitative and quantitative research in developmental science: uses and methodological choices

Multiple methods are vital to understanding development as a dynamic, transactional process. This article focuses on the ways in which quantitative and qualitative methodologies can be combined to enrich developmental science and the study of human development, focusing on the practical questions of "when" and "how." Research situations that may be especially suited to mixing qualitative and quantitative approaches are described. The authors also discuss potential choices for using mixed quantitative- qualitative approaches in study design, sampling, construction of measures or interview protocols, collaborations, and data analysis relevant to developmental science. Finally, they discuss some common pitfalls that occur in mixing these methods and include suggestions for surmounting them.     

Toward computational neuroconstructivism: a framework for developmental systems neuroscience

Brain development is underpinned by complex interactions between neural assemblies, driving structural and functional change. This neuroconstructivism (the notion that neural functions are shaped by these interactions) is core to some developmental theories. However, due to their complexity, understanding underlying developmental mechanisms is challenging. Elsewhere in neurobiology, a computational revolution has shown that mathematical models of hidden biological mechanisms can bridge observations with theory building. Can we build a similar computational framework yielding mechanistic insights for brain development? Here, we outline the conceptual and technical challenges of addressing this theory gap, and demonstrate that there is great potential in specifying brain development as mathematically defined processes operating within physical constraints. We provide examples, alongside broader ingredients needed, as the field explores computational explanations of system-wide development.     

Plasticity of nonneuronal brain tissue: roles in developmental disorders

Neuronal and nonneuronal plasticity are both affected by environmental and experiential factors. Remodeling of existing neurons induced by such factors has been observed throughout the brain, and includes alterations in dendritic field dimensions, synaptogenesis, and synaptic morphology. The brain loci affected by these plastic neuronal changes are dependent on the type of experience and learning. Increased neurogenesis in the hippocampal dentate gyrus is a well-documented response to environmental complexity ("enrichment") and learning. Exposure to challenging experiences and learning opportunities also alters existing glial cells (i.e., astrocytes and oligodendrocytes), and up-regulates gliogenesis, in the cerebral cortex and cerebellum. Such glial plasticity often parallels neuronal remodeling in both time and place, and this enhanced morphological synergism may be important for optimizing the functional interaction between glial cells and neurons. Aberrant structural plasticity of nonneuronal elements is a contributing factor, as is aberrant neuron plasticity, to neurological and developmental disorders such as epilepsy, autism, and mental retardation (i.e., fragile X syndrome). Some of these nonneuronal pathologies include abnormal cerebral and cerebellar white matter and myelin-related proteins in autism; abnormal myelin basic protein in fragile X syndrome (FXS); and abnormal astrocytes in autism, FXS, and epilepsy. A number of recent studies demonstrate the possibility of using environmental and experiential intervention to reduce or ameliorate some of the neuronal and nonneuronal abnormalities, as well as behavioral deficits, present in these neurological and developmental disorders.     

Adult attachment and Mindfulness: Examining directionality,causality, and theoretical implications

We present two studies that together provide preliminary evidence to challenge the view that the relationship between adult attachment and mindfulness is bi-directional (Study 1: repeated measures design and Study 2: a repeated measures study examining the efficacy of attachment security priming and a mindfulness induction). Adult attachment anxiety emerged as a significant predictor of some facets of mindfulness, over time, but the reverse was not true. Priming attachment security increased state mindfulness of mind to a greater degree than a mindfulness induction or control. These findings challenge previous research suggesting that the relationship between adult attachment and mindfulness is bi-directional, suggesting that attachment orientation plays a causal role in the development of mindfulness.     

Why specific developmental disorders are not specific: On-line and developmental effects in autism and dyslexia

In this paper we will suggest that impairments in domain-specific functions may have wide-ranging developmental effects which mimic domain-general impairments. This may explain why ‘pure’ cases of developmental disorders are rare. The understanding of autism and dyslexia has been advanced by theories postulating failure of a specific mechanism against a background of unimpaired general processing. Impairment in the mechanisms underlying ‘theory of mind’ in autism, and ‘phonology’ in dyslexia, predict and explain the pattern of poor and good performance on a range of experimental and real-life tasks. However, existing accounts deal largely with the on-line effects of modular deficits, and can be criticised as not truly developmental. Here we attempt to trace developmental or down-stream effects of specific impairments in mentalising and phonological processing. We argue that these modules act as vital gatekeepers in development. Important in this process is the interaction of cognition with socio-cultural environment, an effect well-illustrated by cross-language differences in dyslexia. We claim that consideration of these developmental effects makes clear why postulating specific impairments may be sufficient for explaining more general deficits.     

Growth mixture modelling in developmental psychology: overview and demonstration of heterogeneity in developmental trajectories of adolescent antisocial behaviour

Recent advances in statistical techniques for longitudinal data analysis have provided increased capabilities for elucidating individual differences in trajectories of change in child behaviours and abilities. However, most techniques still assume that there is a single underlying distribution with respect to changes over time, about which children are normally distributed. If there are multiple subgroups of youth following distinct developmental trajectories with unique predictors, however, the results of these statistical techniques may provide an incomplete analysis of the data. A newer class of statistical techniques, latent growth mixture modelling, provides a robust framework for examining heterogeneity in patterns of development. This paper illustrates the use of latent growth mixture modelling for examining heterogeneity in developmental trajectories of adolescent antisocial behaviour. Copyright © 2006 John Wiley & Sons, Ltd.     

Cognitive processes in university learning: A developmental framework using structural equation modelling

Background. Both achievement goals and study processing strategies theories have been shown to contribute to the prediction of students’ academic performance. Existing research studies ( Fenollar, Román, & Cuestas, 2007 ; Liem, Lau, & Nie, 2008 ; Simons, Dewitte, & Lens, 2004 ) amalgamating these two theoretical orientations in different causal models have reported their associations with other adaptive strategies and motivational constructs – for example, effort expenditure. Despite this recognition, there have been to date very few studies that explored the relations between achievement goals, study processing strategies, effort, and academic performance over time. Aim of study. The primary focus of our study is to explore the relations between the aforementioned theoretical constructs over a 2‐year period. Specifically, we tested an empirical model that conceptualized the relations between performance‐approach and mastery goals, deep processing strategies, effort, and academic performance across six time points of data collection. Methodology. Two hundred and eighty‐one (161 females, 120 males) university students took part in this study. The participants were administered various Likert‐scale inventories and the overall course mark and final examination were used as indexes of academic performance. Results. Structural equation modelling indicated a relatively good fit to the a posteriori model and the hypothesized paths were, in part, supported. The major findings included the predictive effects of performance‐approach goals at Time 1 on deep processing strategies at Time 2 and mastery goals at Time 3; the predictive effect of mastery goals at Time 3 on effort at Time 4; the predictive effects of deep processing at Time 2 on mastery goals at Time 3 and Time 4. Furthermore, the placement of deep processing and effort in this structural model also accentuated the performance‐approach goals – mastery goals – effort – academic performance relation, and the performance‐approach goals – deep processing – mastery goals – effort – academic performance relation. Discussion. Our study has important theoretical and practical implications concerning the conceptualization of the performance‐approach and mastery goals relationship, and the use of goal structure and adaptive strategies (e.g., deep processing) to enhance academic learning.     

Forgetting of stimulus attributes: methodological implications for assessing associative phenomena.

Differential responding to changes in the stimulus situation, long central to the concept of stimulus control, also provides the implicit conceptual basis for assessing the nature of a variety of associative relationships. However, there is substantial evidence that the perception of stimulus similarity is not a static property. Generalization gradients to contextual as well as discriminative stimuli flatten over time, and this increase in perceived similarity presumably reflects forgetting of the detailed characteristics or attributes of stimuli. Methodologically, the flattening of the gradient imposes an important constraint: The effect of a stimulus shift will be highly sensitive to the length of the delay interval between training and testing. Conceptually, the loss of memory for stimulus attributes also implies that the sources of interference in retention can increase over time.     

Placebo effects in developmental disabilities: implications for research and practice

Recent clinical trials of secretin in children with autism showed robust placebo effects and no benefit of secretin over placebo. This article explores the reasons for the observed placebo effects, focusing on the heightening of positive expectancy by media attention and by the sensory experiences associated with intravenous injections. Comparisons are drawn with research involving other novel treatments and other clinical populations of children with developmental disabilities and neurobehavioral disorders. Research regarding mechanisms of placebo effects is reviewed, including patient and clinician attributes, expectancy effects, participation effects, changes in caregiver behavior, and conditioning. New evidence regarding the biological basis of placebo effects is briefly presented. Since placebo effects are ubiquitous and may operate by a variety of mechanisms, research design is critical in designing clinical trials and in evaluating other outcomes research. Measurement issues important for research in developmental disabilities are emphasized. Ethical concerns have been raised regarding the use of placebo in clinical research, but current analysis suggests that placebo controls are necessary and defensible on ethical grounds, if certain conditions are met. The study of placebo effects ("placebology") holds great promise as a new area of research in therapeutics. The author's research in the potential augmentation of stimulant effects in children with attention deficit/hyperactivity disorder (ADHD) by adding placebo in open label is briefly presented. The placebo has always been integral to the practice of medicine, but advances in scientific medicine and medical ethics have diminished the role and use of placebo in practice. An innovative approach to the ethical use of placebo is proposed.     

Co-occurrence of developmental disorders: The case of Developmental Dyscalculia

Five to seven percent of children experience severe difficulties in learning mathematics and/or reading. Current trials that are focused on identifying biological markers suggest that these learning disabilities, known as Developmental Dyscalculia (DD) and Dyslexia (for reading), are due to underlying brain dysfunctions. One ongoing controversy concerns the extent to which arithmetic impairments are specific to DD or shared with other developmental disorders such as Dyslexia. This review explores and develops a hypothesis for cases of DD + Dyslexia. Three factors warrant consideration: (a) the behavioral factor, including definitions of the disabilities and assessment tools; (b) the cognitive factor, including whether co-occurrence of DD and other developmental disorders such as Dyslexia derive from similar or different cognitive risk factors; (c) the biological factor, including consideration of static vs. developmental neuropsychology. Better understanding of the causes of co-occurrence of DD and Dyslexia, or other developmental disorder such as Attention Deficit Hyperactivity Disorder (ADHD), can have an important influence on research that examine the two disorders, including research on therapy and etiology.     

Pervasive developmental disorders rating scale: development and construct validity

The Pervasive Developmental Disorders Rating Scale was designed for use in screening of pervasive developmental disorders. This paper describes the rationale and development of the scale and assesses its construct validity with ratings from a sample of 362 children ranging in age from 1 to 12 years and diagnosed with autistic disorder. The hypothesized heirarchical factor model and two competing models were examined through confirmatory factor analysis. The analysis supported the factor structure of the hypothesized model in this particular sample of children with autistic disorder. Limitations and areas for research are discussed.