Developmental Dyslexia Peterson, Robin L; Pennington, Bruce F
Annual review of clinical psychology,
03/2015, Volume:
11, Issue:
1
Journal Article
Peer reviewed
This review uses a levels-of-analysis framework to summarize the current understanding of developmental dyslexia's etiology, brain bases, neuropsychology, and social context. Dyslexia is caused by ...multiple genetic and environmental risk factors as well as their interplay. Several candidate genes have been identified in the past decade. At the brain level, dyslexia is associated with aberrant structure and function, particularly in left hemisphere reading language networks. The neurocognitive influences on dyslexia are also multifactorial and involve phonological processing deficits as well as weaknesses in other oral language skills and processing speed. We address contextual issues such as how dyslexia manifests across languages and social classes as well as what treatments are best supported. Throughout the review, we highlight exciting new research that cuts across levels of analysis. Such work promises eventually to provide a comprehensive explanation of the disorder as well as its prevention and remediation.
Developmental dyslexia Peterson, Robin L, PhD; Pennington, Bruce F, PhD
The Lancet,
05/2012, Volume:
379, Issue:
9830
Journal Article
Peer reviewed
Open access
Summary Dyslexia is a neurodevelopmental disorder that is characterised by slow and inaccurate word recognition. Dyslexia has been reported in every culture studied, and mounting evidence draws ...attention to cross-linguistic similarity in its neurobiological and neurocognitive bases. Much progress has been made across research specialties spanning the behavioural, neuropsychological, neurobiological, and causal levels of analysis in the past 5 years. From a neuropsychological perspective, the phonological theory remains the most compelling, although phonological problems also interact with other cognitive risk factors. Work confirms that, neurobiologically, dyslexia is characterised by dysfunction of the normal left hemisphere language network and also implicates abnormal white matter development. Studies accounting for reading experience demonstrate that many recorded neural differences show causes rather than effects of dyslexia. Six predisposing candidate genes have been identified, and evidence shows gene by environment interaction.
The emerging etiological model for developmental disorders, like dyslexia, is probabilistic and multifactorial while the prevailing cognitive model has been deterministic and often focused on a ...single cognitive cause, such as a phonological deficit as the cause of dyslexia. So there is a potential contradiction in our explanatory frameworks for understanding developmental disorders. This paper attempts to resolve this contradiction by presenting a multiple cognitive deficit model of developmental disorders. It describes how this model evolved out of our attempts to understand two comorbidities, those between dyslexia and attention deficit hyperactivity disorder (ADHD) and between dyslexia and speech sound disorder (SSD).
Sex differences in ADHD symptom severity Arnett, Anne B.; Pennington, Bruce F.; Willcutt, Erik G. ...
Journal of child psychology and psychiatry,
June 2015, Volume:
56, Issue:
6
Journal Article
Peer reviewed
Open access
Background
Males show higher rates of attention deficit hyperactivity disorder (ADHD) than do females. Potential explanations include genuine etiological differences or artifact.
Methods
2,332 twin ...and sibling youth participated in behavioral and cognitive testing. Partially competing models of symptom severity distribution differences, the mean difference, and variance difference models, were tested within a randomly selected subsample. The Delta method was used to test for mediation of sex differences in ADHD symptom severity by processing speed, inhibition and working memory.
Results
The combined mean difference and variance difference models fully explained the sex difference in ADHD symptom severity. Cognitive endophenotypes mediated 14% of the sex difference effect.
Conclusions
The sex difference in ADHD symptom severity is valid and may be due to differing genetic and cognitive liabilities between the sexes.
One of the most prominent neuropsychologic theories of attention-deficit/hyperactivity disorder (ADHD) suggests that its symptoms arise from a primary deficit in executive functions (EF), defined as ...neurocognitive processes that maintain an appropriate problem-solving set to attain a later goal. To examine the validity of the EF theory, we conducted a meta-analysis of 83 studies that administered EF measures to groups with ADHD (total
N = 3734) and without ADHD (
N = 2969). Groups with ADHD exhibited significant impairment on all EF tasks. Effect sizes for all measures fell in the medium range (.46–.69), but the strongest and most consistent effects were obtained on measures of response inhibition, vigilance, working memory, and planning. Weaknesses in EF were significant in both clinic-referred and community samples and were not explained by group differences in intelligence, academic achievement, or symptoms of other disorders. ADHD is associated with significant weaknesses in several key EF domains. However, moderate effect sizes and lack of universality of EF deficits among individuals with ADHD suggest that EF weaknesses are neither necessary nor sufficient to cause all cases of ADHD. Difficulties with EF appear to be one important component of the complex neuropsychology of ADHD.
The multiple deficit model (MDM) was proposed because the prevailing single deficit model provided an inadequate account of atypical neuropsychological development. Across methods and levels of ...analysis, there has been support for the two fundamental tenets of the MDM, that multiple predictors contribute probabilistically to neurodevelopmental disorders and shared risk factors contribute to comorbidity. Diagnostically, the multiplicity of factors means that no single cognitive deficit or combination of deficits can be used to rule in or out most neurodevelopmental disorders. Challenges for the MDM are that the theory is difficult to falsify and that current cross-sectional studies cannot establish causality. Prospects for further development of the MDM include incorporating an explicit focus on promotive and protective factors and pursuing mechanistic connections between multiple factors across levels of analysis.
Explaining the sex difference in dyslexia Arnett, Anne B.; Pennington, Bruce F.; Peterson, Robin L. ...
Journal of child psychology and psychiatry,
June 2017, Volume:
58, Issue:
6
Journal Article
Peer reviewed
Open access
Background
Males are diagnosed with dyslexia more frequently than females, even in epidemiological samples. This may be explained by greater variance in males’ reading performance.
Methods
We expand ...on previous research by rigorously testing the variance difference theory, and testing for mediation of the sex difference by cognitive correlates. We developed an analytic framework that can be applied to group differences in any psychiatric disorder.
Results
Males’ overrepresentation in the low performance tail of the reading distribution was accounted for by mean and variance differences across sex. There was no sex difference at the high performance tail. Processing speed (PS) and inhibitory control partially mediated the sex difference. Verbal reasoning emerged as a strength in males.
Conclusions
Our results complement a previous finding that PS partially mediates the sex difference in symptoms of attention deficit/hyperactivity disorder (ADHD), and helps explain the sex difference in both dyslexia and ADHD and their comorbidity.
Background: This study tests a multiple cognitive deficit model of reading disability (RD), attention‐deficit/hyperactivity disorder (ADHD), and their comorbidity.
Methods: A structural equation ...model (SEM) of multiple cognitive risk factors and symptom outcome variables was constructed. The model included phonological awareness as a unique predictor of RD and response inhibition as a unique predictor of ADHD. Processing speed, naming speed, and verbal working memory were modeled as potential shared cognitive deficits.
Results: Model fit indices from the SEM indicated satisfactory fit. Closer inspection of the path weights revealed that processing speed was the only cognitive variable with significant unique relationships to RD and ADHD dimensions, particularly inattention. Moreover, the significant correlation between reading and inattention was reduced to non‐significance when processing speed was included in the model, suggesting that processing speed primarily accounted for the phenotypic correlation (or comorbidity) between reading and inattention.
Conclusions: This study illustrates the power of a multiple deficit approach to complex developmental disorders and psychopathologies, particularly for exploring comorbidities. The theoretical role of processing speed in the developmental pathways of RD and ADHD and directions for future research are discussed.
In this article, we critically review the evidence for overlap among three developmental disorders, namely speech sound disorder (SSD), language impairment (LI), and reading disability (RD), at three ...levels of analysis: diagnostic, cognitive, and etiological. We find that while overlap exists at all three levels, it varies by comorbidity subtype, and the relations among these three disorders are complex and not fully understood. We evaluate which comorbidity models can be rejected or supported as explanations for why and how these three disorders overlap and what new data are needed to better define their relations.
This study tested prefrontal and hippocampal functions in a sample of 28 school-aged (M = 14.7 years, SD = 2.7) individuals with Down syndrome (DS) compared with 28 (M = 4.9 years, SD = .75) ...typically developing children individually matched on mental age (MA). Both neuropsychological domains were tested with multiple behavioral measures. Benchmark measures of verbal and spatial function demonstrated that this DS sample was similar to others in the literature. The main finding was a significant Group x Domain interaction effect indicating differential hippocampal dysfunction in the group with DS. However, there was a moderate partial correlation (r = .54, controlling for chronological age) between hippocampal and prefrontal composite scores in the DS group, and both composites contributed unique variance to the prediction of MA and adaptive behavior in that group. In sum, these results indicate a particular weakness in hippocampal functions in DS in the context of overall cognitive dysfunction. It is interesting that these results are similar to what has been found in a mouse model of DS. Such a model will make it easier to understand the neurobiological mechanisms that lead to the development of hippocampal dysfunction in DS.
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