Jeffrey W. Gilger

A Twin Study of the Etiology of Comorbidity: Attention-deficit Hyperactivity Disorder and Dyslexia

Monozygotic and dizygotic twin pairs, in which at least one member of each pair is reading disabled (RD), were assessed for attention-deficit hyperactivity disorder (ADHD). Within pair cross-concordances of the RD and ADHD qualitative diagnoses for monozygotic twins were larger than for dizygotic twins, although not significantly so (p less than 0.10). Thus, the data suggest that RD and ADHD may be primarily genetically independent. However, trends in the data and subtype analyses suggest that in some cases RD and ADHD may occur together because of a shared genetic etiology and that a genetically mediated comorbid subtype may exist.

Attention deficit disorder in reading-disabled twins: Evidence for a genetic etiology

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.

Atypical Brain Development: A Conceptual Framework for Understanding Developmental Learning Disabilities

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.

Risk for Reading Disability as a Function of Parental History in Three Family Studies

Inverse Bayesian analyses were applied to data from three large family studies of reading disability to estimate the posterior probability that an offspring will be affected, given that a parent reported a history of learning problems. Prior analyses presented elsewhere (Pennington et al., 1990), suggest that family transmission in these three studies is consistent with major gene or polygene influence. Posterior probability rates are presented in this paper for male to female sex ratios of 3.5:1 and 1:1, with population incidences estimated at 0.05 and 0.10. Results indicate that offspring risk rates are significantly elevated if a parent reports a history of RD. Specifically, an offsprings risk was increased 2 to 80 times over population expectancies when there was an affected parent. While the posterior probabilities and relative risk rates were fairly similar across studies, there was also some variation, which may reflect the different genetic mechanisms operating in these families. This study concludes that both absolute and relative risks are sufficiently increased in families with RD parents to warrant use of family history as a component in clinical evaluation. It is also evident from these results that consideration of the apparent mode of genetic transmission in families may provide even better information as to offspring risk, when family history is obtained.

The External Validity of Age- Versus IQ-Discrepancy Definitions of Reading Disability Lessons From a Twin Study

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.

Reading disability and hyperactivity disorder: Evidence for a common genetic etiology

In order to assess the genetic etiology of comorbid reading disability and attention deficit hyperactivity disorder (ADHD), reading performance and hyperactivity data (Diagnostic Interview for Children and Adolescents [DICA]; Herjanic, Campbell, & Reich, 1982) from 61 identical and 43 same‐sex fraternal twin pairs tested in the Colorado Reading Project were subjected to multiple‐regression analysis (DeFries & Fulker, 1985, 1988). Results suggest that approximately 45% of the proband deficit in reading is due to genetic factors that also influence hyperactivity. Moreover, heritable variation accounted for 70% of the observed covariance between the reading and hyperactivity measures. Thus, comorbid reading disability and ADHD (as measured by parental ratings on the DICA) is due, at least in part, to heritable influences.

Gender differences in adult spatial information processing: Their relationship to pubertal timing, adolescent activities, and sex-typing of personality ☆

Abstract This study explored the contributions of pubertal timing, sex-role orientation, and childhood experiences to gender differences in adult spatial ability. Two-dimensional spatial orientation ability was assessed in 52 female and 38 male college students with both information-processing and paper-and-pencil tasks. Retrospective indices of pubertal timing and previous experiences with spatial-related activities, as well as measures of the subjects adult sex-role orientation were also obtained. The direction of influence inferred from the pattern of mean differences and the results of simple and multiple regression analyses suggest that gender differences in mental rotation rate as assessed by the information-processing measure are linked to gender differences in spatial-related adolescent experiences, and to a lesser extent, adolescent pubertal timing. On the other hand, gender differences in test accuracy did not appear to be significantly related to gender differences in maturational timing, adolescent activities, or adult sex-role orientation. Implications of these findings for the locus of gender differences in spatial ability and its potentially experiential nature are discussed.

Reading disability, immune disorders and non-right-handedness: Twin and family studies of their relations

Geschwind and colleagues discussed associations among learning disorders, immune disorders and non-right-handedness. In this study, we examined the associations between reading disability (RD) and both immune disorders (ID) and non-right-handedness (NRH) in family and twin samples (total N = 1731 cases) identified through an RD proband. We also conducted co-segregation analyses to ascertain the degree to which NRH, ID and RD were biologically related. There was little evidence for an overall association between RD and NRH. There was not convergent evidence across all four samples for an association between RD and ID, although we did find an association between RD and ID in two of four samples. Nor was there strong support for a subtype where RD and NRH, or RD and ID, co-segregate in families. These data suggest that the associations postulated by Geschwind and colleagues are not robust in RD samples, although we cannot completely rule out the possibility of an RD plus ID subtype.

Commingling and segregation analysis of reading performance in families of normal reading probands

This paper reports the results of commingling and genetic segregation analyses performed on a quantitative reading phenotype in 125 families ascertained through normal, nondisabled readers. Commingling analysis using SKUMIX suggested that the reading phenotype best fit a skewed, single distribution model. Complex segregation using POINTER was then performed on the power adjusted data. While there were some analytical ambiguities and complexities, the segregation analysis indicated that there was familial transmission of the phenotype and that a significant percentage of the variance in this phenotype could be attributed to a major gene with dominance. Because the estimated frequency of the putative dominant allele is 35, 57% of the population would carry at least one copy of this allele. This common allele, with low penetrance, accounted for 54% of the phenotypic variance in reading scores. These findings are considered in the context of our earlier report of major gene influence on a qualitative dyslexic phenotype in a sample of 133 dyslexic proband families that were originally matched to the present sample of control families (Penningtonet al., 1991). The applicability of a classic single gene, multifactorial-polygenic, and oligogenic or QTL models for reading ability/disability is discussed.

THE LURIA-NEBRASKA NEUROPSYCHOLOGICAL BATTERY-CHILDREN'S REVISION: COMPARISON OF LEARNING DISABLED AND NORMAL CHILDREN MATCHED ON FULL SCALE IQ

17 academically normal and 17 reading disabled children were matched on Full Scale IQ and compared on the Luria-Nebraska Neuropsychological Battery—Childrens Revision. The academically normal group performed significantly better on the Expressive Language, Writing, Reading, and Rhythm subscales, which suggests that the Luria-Nebraska may be sensitive to deficits not reflected in Full Scale IQ. Results are consistent with previous research and support the validity of the Luria-Nebraska, although simplistic interpretation of the batterys subscales should be avoided.