Measures of component reading and language skills, executive functions, and processing speed were administered to groups of children with attention deficit hyperactivity disorder (ADHD; n = 113), reading disability (RD; n = 109), both RD and ADHD (n = 64), and neither RD nor ADHD (n = 151). Groups with RD exhibited pronounced deficits on all measures of component reading and language skills, as well as significant weaknesses on measures of verbal working memory, processing speed, and response inhibition. Groups with ADHD exhibited weaknesses on all response-inhibition and processing speed tasks and were impaired on some measures of component reading skills and verbal working memory. The group with comorbid RD and ADHD exhibited the combination of the deficits in the RD-only and ADHD-only groups, providing evidence against the phenocopy and cognitive subtype hypotheses as explanations for the co-occurrence of RD and ADHD. Slow and variable processing speed was characteristic of all 3 clinical groups, suggesting that measures of this domain may be useful for future studies that search for the common genes that increase susceptibility to RD and ADHD.

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.

Introduction-Attention-deficit/hyperactivity disorder (ADHD) and reading disability (RD) are complex childhood disorders that frequently co-occur, but the etiology of this comorbidity remains unknown.Method-Participants were 457 twin pairs from the Colorado Learning Disabilities Research Center (CLDRC) twin study, an ongoing study of the etiology of RD, ADHD, and related disorders. Phenotypic analyses compared groups with and without RD and ADHD on composite measures of six cognitive domains. Twin analyses were then used to test the etiology of the relations between the disorders and any cognitive weaknesses.Results-Phenotypic analyses supported the hypothesis that both RD and ADHD arise from multiple cognitive deficits rather than a single primary cognitive deficit. RD was associated independently with weaknesses on measures of phoneme awareness, verbal reasoning, and working memory, whereas ADHD was independently associated with a heritable weakness in inhibitory control. RD and ADHD share a common cognitive deficit in processing speed, and twin analyses indicated that this shared weakness is primarily due to common genetic influences that increase susceptibility to both disorders.Conclusions-Individual differences in processing speed are influenced by genes that also increase risk for RD, ADHD, and their comorbidity. These results suggest that processing speed measures may be useful for future molecular genetic studies of the etiology of comorbidity between RD and ADHD.

Studies of subtypes of DSM-IV attention-deficit/hyperactivity disorder (ADHD) have provided inconsistent support for the discriminant validity of the combined type (ADHD-C) and predominantly inattentive type (ADHD-I). A large sample of children and adolescents with ADHD (N = 410) and a comparison group without ADHD (N = 311) were used to test the internal and external validity of sluggish cognitive tempo (SCT), a dimension characterized by low energy and sleepy and sluggish behavior. SCT scores were then incorporated in analyses of ADHD subtypes to test whether the discriminant validity of ADHD-C and ADHD-Icould be improved by includingSCT symptoms as part of the criteria for ADHD-I. Factor analyses of parent and teacher ratings indicated that six SCT items loaded on a factor separate from symptoms of ADHD and other psychopathology, providing important support for the internal validity of SCT. The external validity of SCT was supported by significant associationsbetween SCT and measures of functional impairment and neuropsychological functioning when symptoms of ADHD and other psychopathology were controlled. However, contrary to initial predictions, high levels of SCT did not identify a subgroup of ADHD-I that was clearly distinct from ADHD-C. Instead, the current results suggest that DSM-IV inattention and SCT are separate but correlated symptom dimensions that are each independently associated with important aspects of functional impairment and neuropsychological functioning.

Although it is well known that there is considerable variation among individuals in the size of the human brain, the etiology of less extreme individual differences in brain size is largely unknown. We present here data from the first large twin sample (N=132 individuals) in which the size of brain structures has been measured. As part of an ongoing project examining the brain correlates of reading disability (RD), whole brain morphometric analyses of structural magnetic response image (MRI) scans were performed on a sample of adolescent twins. Specifically, there were 25 monozygotic (MZ) and 23 dizygotic (DZ) pairs in which at least one member of each pair had RD and 9 MZ and 9 DZ pairs in which neither member had RD. We first factor-analyzed volume data for 13 individual brain structures, comprising all of the neocortex and most of the subcortex. This analysis yielded two factors ("cortical" and "subcortical") that accounted for 64% of the variance. We next tested whether genetic and environmental influences on brain size variations varied for these two factors or by hemisphere. We computed intraclass correlations within MZ and DZ pairs in each sample for the cortical and subcortical factor scores, for left and right neocortex, and for the total cerebral volume. All five MZ correlations were substantial (r's=.78 to.98) and significant in both samples, as well as being larger than the corresponding DZ correlations, (r's=0.32 to 0.65) in both samples. The MZ-DZ difference was significant for 3 variables in the RD sample and for one variable in the smaller control sample. These results indicate significant genetic influences on these variables. The magnitude of genetic influence did not vary markedly either for the 2 factors or the 2 hemispheres. There was also a positive correlation between brain size and full-scale IQ, consistent with the results of earlier studies. The total cerebral volume was moderately correlated (r=.42, p<.01, two-tailed) with full-scale IQ in the RD sample; there was a similar trend in the smaller control sample (r=.31, p<.07, two-tailed). Corrections of similar magnitude were found between the subcortical factor and full-scale IQ, whereas the results for the cortical factor (r=.16 and.13) were smaller and not significant. In sum, these results provide evidence for the heritability of individual differences in brain size which do not vary markedly by hemisphere or for neocortex relative to subcortex. Since there are also correlations between brain size and full-scale IQ in this sample, it is possible that genetic influences on brain size partly contribute to individual differences in IQ.