In a 3-year longitudinal study, middle- to upper-middle-class preschool children at high family risk (HR group, N = 67) and low family risk (LR group, N = 57) for dyslexia (or reading disability, RD), were evaluated yearly from before kindergarten to the end of second grade. Both phonological processing and literacy skills were tested at each of four time points. Consistent with the well-known familiarity of RD, 34% of the HR group compared with 6% of the LR group became RD. Participants who became RD showed deficits in both implicit and explicit phonological processing skills at all four time points, clearly indicating a broader phonological deficit than is often found at older ages. The predictors of literacy skill did not vary by risk group. Both risk groups underwent a similar developmental shift from letter-name knowledge to phoneme awareness as the main predictor of later literacy skill. This shift, however, occurred 2 years later in the HR group. Familial risk was continuous rather than discrete because HR children who did not become RD performed worse than LR non-RD children on some phonological and literacy measures. Finally, later RD could be predicted with moderate accuracy at age 5 years, with the strongest predictor being letter-name knowledge.

The reliability and validity of a revised version of Finucci's (1982) Reading History Questionnaire was examined in two adult samples. One sample included 84 adults from an ongoing study of familial dyslexia, and a second sample was composed of parents of 107 children from a longitudinal study of reading development. Internal consistency was demonstrated by Cronbach's alphas of .94 and .92 in the two samples. Test-retest reliability was demonstrated by significant correlations (.87 and .84 in the two samples) over several years between an earlier and revised form of the questionnaire. Validity was demonstrated via (a) correlations between the questionnaire score and reading measures (rs = .57-.70), (b) the results of a discriminant function analysis that used questionnaire scores to predict reading disability diagnosis, and (c) the finding that the questionnaire had substantial incremental validity in predicting reading skill in a hierarchical regression analysis that first entered IQ and SES. These results indicated that the questionnaire is both reliable and valid.

Generally, a person who is diagnosed as dyslexic remains diagnosably dyslexic all his/her life. However, occasionally, an individual compensates for his/her difficulties in some way, and by adulthood is no longer diagnosably dyslexic. In what ways are these compensated dyslexics different from both dyslexics and nondyslexics? We compared IQ, achievement test, and spelling error scores in adult dyslexics, adult nondyslexics, and adult compensated dyslexics (N=25) in the two studies reported here. The second study differed from the first in that the subjects were matched for age, education, IQ, and SES. In both studies, compensateds were significantly different from nondyslexics on the WRAT Spelling subtest and Reading Quotient scores. In the second study the compensateds differed from the nondyslexics in total raw score and average reading speed on Gray Oral Reading Test. On the other hand, they were different from dyslexics on all reading and spelling variables in both studies, except for PIAT Reading Comprehension in Study 2. Finally, in Study 2, the compensateds were different from both dyslexics and nondyslexics in average reading speed. In conclusion, it appears that compensation does not result from differences in IQ, education, or SES, though it may be influenced to some extent by sex. Compensateds appear very similar to nondyslexics in their reading and spelling skills; however, there appears to be a difference in the automaticity with which they apply these skills.

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.

We compared the spelling errors on the WRAT II made by adults (N = 24) with an apparent autosomal dominant form of dyslexia to those made by their normal adult relatives (N = 17) and by spelling-age matched normal controls (N = 17) using a computerized error evaluation program (SEEP). The normal adult relatives were significantly better than the dyslexics in both reading and spelling, but did not differ in age, education, or IQ. SEEP evaluated each error independently for both phonological and orthographic accuracy at 2 levels of complexity. Each level of complexity was analyzed separately using a 3 X 2 (group X dimension) analysis of variance. The main finding of interest was a significant group X dimension interaction effect at the complex level, which indicated that the dyslexics had a qualitatively different profile across the 2 dimensions than either normal group who had parallel profiles. The dyslexics performed like the younger normal group on the complex phonological dimension but like the adult normal group on the complex orthographic dimension. These results indicate a dissociation in this form of familial dyslexia between these 2 dimensions of spelling development, and suggest that these dyslexics may fit the subtype of dysphonetic or phonological dyslexia. The implications of these results for the underlying cognitive deficit in this form of dyslexia are discussed.