This study used a nonreferred sample of twins to contrast the performance of individuals with reading disability (RD; n = 93), attention-deficit/hyperactivity disorder (ADHD; n = 52), RD and ADHD (n = 48), and neither RD nor ADHD (n = 121) on measures of phoneme awareness (PA) and executive functioning (EF). Exploratory factor analysis of the EF measures yielded underlying factors of working memory, inhibition, and set shifting. Results revealed that ADHD was associated with inhibition deficits, whereas RD was associated with significant deficits on measures of PA and verbal working memory. The RD + ADHD group was most impaired on virtually all measures, providing evidence against the phenocopy hypothesis as an explanation for comorbidity between RD and ADHD.
The goal of the current study was to test whether deficits in processing speed (PS) may be a shared cognitive risk factor in reading disability (RD) and Attention Deficit/Hyperactivity Disorder (ADHD), which are known to be comorbid. Literature on ADHD and RD suggests that deficits on tasks with a speeded component are seen in both of these disorders individually. The current study examined a wide range of speeded tasks in RD, ADHD, comorbid RD+ADHD, and a control group to test whether RD and ADHD have similar profiles of PS deficits, and whether these deficits are shared by the two disorders. The results suggest that a general PS deficit exists in both clinical groups compared to controls, although children with RD demonstrate greater PS deficits than children with ADHD. Two tests (underadditivity and partial correlations) were conducted to test whether these PS deficits are shared. Since we found that PS deficits were underadditive in the comorbid group and that partialling PS reduced the correlation between RD and ADHD, it appears that PS is a shared cognitive risk factor that may help explain the comorbidity of these two disorders.
The overall goals of this study were to test single vs. multiple cognitive deficit models of dyslexia (reading disability) at the level of individual cases and to determine the clinical utility of these models for prediction and diagnosis of dyslexia. To accomplish these goals, we tested five cognitive models of dyslexia: two single-deficit models, two multiple-deficit models, and one hybrid model in two large population-based samples, one cross-sectional (Colorado Learning Disability Research Center—CLDRC) and one longitudinal (International longitudinal Twin Study—ILTS). The cognitive deficits included in these cognitive models were in phonological awareness, language skill, and processing speed and/ or naming speed. To determine whether an individual case fit one of these models, we used two methods: 1) the presence or absence of the predicted cognitive deficits, and 2) whether the individual’s level of reading skill best fit the regression equation with the relevant cognitive predictors (i.e. whether their reading skill was proportional to those cognitive predictors.) We found that roughly equal proportions of cases met both tests of model fit for the multiple deficit models (30–36%) and single deficit models (24–28%); hence, the hybrid model provided the best overall fit to the data. The remaining roughly 40% of cases in each sample lacked the deficit or deficits that corresponded with their best fitting regression model. We discuss the clinical implications of these results for both diagnosis of school age children and preschool prediction of children at risk for dyslexia.
Reading disability (RD) and Math Disability (MD) frequently co-occur, but the etiology of this comorbidity is not well understood. Groups with RD only (N = 241), MD only (N = 183), RD+MD (N = 188), and a control group with neither disorder (N = 411) completed a battery of measures of internalizing and externalizing psychopathology, social and academic functioning, and ten neuropsychological processes. Groups with RD only, MD only, and RD+MD were significantly impaired versus the control group on nearly all measures, and the group with RD+MD was more impaired than the groups with MD and RD alone on measures of internalizing psychopathology, academic functioning, and seven of ten neuropsychological constructs. Multiple regression analyses of the neuropsychological measures indicated that deficits in reading and math were associated with shared weaknesses in working memory, processing speed, and verbal comprehension. In contrast, reading difficulties were uniquely associated with weaknesses in phoneme awareness and naming speed, and math deficits were uniquely associated with weaknesses in set shifting. These results support multiple-deficit neuropsychological models of RD and MD, and suggest that RD and MD are distinct but related disorders that co-occur due to shared neuropsychological weaknesses in working memory, processing speed, and verbal comprehension.
Background:The existing literature has conflicting findings about the literacy outcome of children with speech sound disorders (SSD), which may be due to the heterogeneity within SSD. Previous studies have documented that two important dimensions of heterogeneity are the presence of a comorbid language impairment (LI) and the persistence of SSD, but these factors have not been examined separately. Method: The current study used a 2 · 2 MANOVA design (with follow-up MANCOVAs) to examine how a comorbid language impairment (LI) and the persistence of SSD relate to pre-literacy skills in a sample of 5-to 6-year-old children with SSD. Results: Significant main effects for persistent SSD and LI were obtained, such that each factor was associated with worse performance on pre-literacy tasks, particularly those assessing phonological awareness (even with nonverbal IQ covaried). In addition, even SSD children with normalized speech without LI were found to have deficits on phonological awareness tasks relative to control participants. Conclusions: These results suggest that a history of SSD and comorbid LI are strong correlates of pre-literacy deficits.
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