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The influence of genetic factors in the comorbidity of spelling disability and hyperactivity was investigated in two samples of 190 and 260 same sex twin pairs. The method of bivariate group heritability was used to estimate the genetic correlation for spelling disability and hyperactivity. A similar though not statistically significant value for the genetic correlation was obtained for the two samples (0.29 and 0.42). It was estimated that approximately 75% of the co-occurrence of these two conditions was due to shared genetic influences.

This article presents ideas that are, in part, a response to the ambiguity in the neurological research on learning disorders, the growing awareness that developmental disabilities are typically nonspecific and heterogeneous, and the growing scientific literature showing that comorbidity of symptoms and syndromes is the rule rather than the exception. This article proposes the term atypical brain development (ABD) as a unifying concept to assist researchers and educators trying to come to terms with these dilemmas. ABD is meant to serve as an integrative concept of etiology, the expression of which is variable within and across individuals. ABD does not itself represent a specific disorder or disease. It is a term that can be used to address the full range of developmental disorders that are found to be overlapping much of the time in any sample of children. Although similar in spirit to the older term of minimal brain dysfunction (MBD), in that it closely links neurology with behavioral difficulties, ABD as proposed here differs in several ways. In support of the ABD conceptual framework, first, we consider the ABD concept in terms of its superiority to the older notion of MBD. Second, we provide a brief review of the burgeoning literature on the overlap of the various developmental disabilities. Third, we review some of the scientific literature that supports the ABD concept. Our sole purpose in proposing this concept is to initiate dialogue and debate on several critical issues across a wide variety disciplines. Hence, this article is not intended to be a definitive statement of a rigid perspective. It reflects neither a nonmalleable philosophical position, nor any type of condemnation of other perspectives. It does, however, reflect a data-based and philosophical trend visible in the field of learning disabilities, as well as the broader area of childhood developmental disorders.

In order to assess the genetic etiology of attention deficit hyperactivity disorder (ADHD), the basic regression model for the analysis of selected twin data (DeFries & Fulker, 1985, 1988) was fitted to questionnaire data (DICA: Diagnostic Interview for Children and Adolescents; Herjanic, Campbell, & Reich, 1982) for 37 identical and 37 fraternal twin pairs tested in the Colorado Reading Project. Results of this analysis suggest that ADHD is highly heritable. Moreover, adjusting DICA scores for either IQ or reading performance differences did not substantially change parameter estimates. In future analyses of larger data sets, distinguishing between possible subtypes of attentional problems (e.g., ADD with or without hyperactivity) may facilitate tests of more searching etiological questions.

Recent research has raised the question of whether age- and IQ-discrepancy forms of reading disability (RD) are distinguishable in terms of either their underlying linguistic deficit or their response to treatment, thus threatening the external validity of the traditional distinction between specific reading retardation and reading backwardness. The present study pursued the external validity of this distinction in three domains: (a) genetic etiology, (b) sex ratio and clinical correlates, and (c) neuropsychological profiles. Each of these domains was explored in the RD (n = 640) and control (n = 436) twins participating in the Colorado Reading Project (514 males, 562 females, with an overall mean age of 12.42 years). Little evidence for external validity was found in terms of the clinical correlates of attention deficit-hyperactivity disorder (ADHD), immune disorders, or handedness. Most importantly, there was no evidence of differential genetic etiology of the two phenotypes in this sample, in that deficits in both phenotypes were similarly heritable (h2g = .40 and .46 for age and IQ phenotypes, respectively) and the genetic correlation between them was high (rG = .88 to .96). However, the genetic and neuropsychological profile analyses did suggest that age- and IQ-discrepancy definitions of RD may relate differentially to component reading processes, such as phonological awareness and orthographic coding.

--Sex-influenced, additive, or dominant transmission occurs in a significant proportion of dyslexic families. Other evidence indicates, however, that dyslexia is etiologically heterogeneous and that there is genetic heterogeneity even among families selected for apparent dominant transmission. Thus, while no single major locus may account for all of dyslexia, it is important to pursue potential major loci for dyslexia using linkage techniques.

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