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This study examined whether domain-general cognitive weaknesses in processing speed (PS) or executive functioning (EF) moderate the relation between word reading scores and anxiety such that lower word reading scores in combination with lower cognitive scores are associated with higher anxiety symptoms. The sample consisted of 755 youth ages 8–16 who were recruited as part of the Colorado Learning Disabilities Research Center twins study. Lower scores on PS (R 2 =.007, p =.014), EF (R 2 =.009, p =.006), and word reading (R 2 =.006–.008, p =.010–.032) were associated with higher anxiety scores. In addition, the word reading × cognitive interactions were significant such that lower scores on PS (R 2 =.010, p =.005) or EF (R 2 =.013, p =.010) combined with lower word reading were associated with higher-than-expected anxiety symptoms. Results suggest that weaknesses in PS, EF, and word reading are modestly associated with higher anxiety symptoms, and these anxiety symptoms may be compounded in youth with both PS or EF weaknesses and word reading difficulties. These findings can guide assessment approaches for identifying youth with word reading challenges who may be at increased risk for anxiety. [ABSTRACT FROM AUTHOR]

Eleven loci with prior evidence for association with reading and language phenotypes were sequenced in 96 unrelated subjects with significant impairment in reading performance drawn from the Colorado Learning Disability Research Center collection. Out of 148 total individual missense variants identified, the chromosome 7 genes CCDC136 and FLNC contained 19. In addition, a region corresponding to the well-known DYX2 locus for RD contained 74 missense variants. Both allele sets were filtered for a minor allele frequency ≤0.01 and high Polyphen-2 scores. To determine if observations of these alleles are occurring more frequently in our cases than expected by chance in aggregate, counts from our sample were compared to the number of observations in the European subset of the 1000 Genomes Project using Fisher's exact test. Significant P values were achieved for both CCDC136/FLNC ( P = 0.0098) and the DYX2 locus ( P = 0.012). Taken together, this evidence further supports the influence of these regions on reading performance. These results also support the influence of rare variants in reading disability. [ABSTRACT FROM AUTHOR]

The current study tested a multiple-cognitive predictor model of word reading, math ability, and attention in a community-based sample of twins ages 8 to 16 years (N = 636). The objective was to identify cognitive predictors unique to each skill domain as well as cognitive predictors shared among skills that could help explain their overlap and thus help illuminate the basis for comorbidity of related disorders (reading disability, math disability, and attention deficit hyperactivity disorder). Results indicated that processing speed contributes to the overlap between reading and attention as well as math and attention, whereas verbal comprehension contributes to the overlap between reading and math. There was no evidence that executive functioning skills help account for covariation among these skill domains. Instead, specific executive functions differentially related to certain outcomes (i.e., working memory to math and inhibition to attention). We explored whether the model varied in younger versus older children and found only minor differences. Results are interpreted within the context of the multiple deficit framework for neurodevelopmental disorders. [ABSTRACT FROM AUTHOR]

Background Reading disability (RD) and language impairment (LI) are heritable learning disabilities that obstruct acquisition and use of written and spoken language, respectively. We previously reported that two risk haplotypes, each in strong linkage disequilibrium (LD) with an allele of READ1, a polymorphic compound short tandem repeat within intron 2 of risk gene DCDC2, are associated with RD and LI. Additionally, we showed a non-additive genetic interaction between READ1 and KIAHap, a previously reported risk haplotype in risk gene KIAA0319, and that READ1 binds the transcriptional regulator ETV6. Objective To examine the hypothesis that READ1 is a transcriptional regulator of KIAA0319. Methods We characterised associations between READ1 alleles and RD and LI in a large European cohort, and also assessed interactions between READ1 and KIAHap and their effect on performance on measures of reading, language and IQ. We also used family-based data to characterise the genetic interaction, and chromatin conformation capture (3C) to investigate the possibility of a physical interaction between READ1 and KIAHap. Results and conclusions READ1 and KIAHap show interdependence--READ1 risk alleles synergise with KIAHap, whereas READ1 protective alleles act epistatically to negate the effects of KIAHap. The family data suggest that these variants interact in trans genetically, while the 3C results show that a region of DCDC2 containing READ1 interacts physically with the region upstream of KIAA0319. These data support a model in which READ1 regulates KIAA0319 expression through KIAHap and in which the additive effects of READ1 and KIAHap alleles are responsible for the trans genetic interaction. [ABSTRACT FROM AUTHOR]

Reading disability (RD) and language impairment (LI) are common neurodevelopmental disorders with moderately strong genetic components and lifelong implications. RD and LI are marked by unexpected difficulty acquiring and processing written and verbal language, respectively, despite adequate opportunity and instruction. RD and LI-and their associated deficits-are complex, multifactorial, and often comorbid. Genetic studies have repeatedly implicated the DYX2 locus, specifically the genes DCDC2 and KIAA0319, in RD, with recent studies suggesting they also influence LI, verbal language, and cognition. Here, we characterize the relationship of the DYX2 locus with RD, LI, and IQ. To accomplish this, we developed a marker panel densely covering the 1.4 Mb DYX2 locus and assessed association with reading, language, and IQ measures in subjects from the Avon Longitudinal Study of Parents and Children. We then replicated associations in three independent, disorder-selected cohorts. As expected, there were associations with known RD risk genes KIAA0319 and DCDC2. In addition, we implicated markers in or near other DYX2 genes, including TDP2, ACOT13, C6orf62, FAM65B, and CMAHP. However, the LD structure of the locus suggests that associations within TDP2, ACOT13, and C6orf62 are capturing a previously reported risk variant in KIAA0319. Our results further substantiate the candidacy of KIAA0319 and DCDC2 as major effector genes in DYX2, while proposing FAM65B and CMAHP as new DYX2 candidate genes. Association of DYX2 with multiple neurobehavioral traits suggests risk variants have functional consequences affecting multiple neurological processes. Future studies should dissect these functional, possibly interactive relationships of DYX2 candidate genes. [ABSTRACT FROM AUTHOR]

Insufficient knowledge of the subtle relations between words' spellings and their phonology is widely held to be the primary limitation in developmental dyslexia. In the present study the influence of phonology on a semantic-based reading task was compared for groups of readers with and without dyslexia. As many studies have shown, skilled readers make phonology-based false-positive errors to homophones and pseudohomophones in the semantic categorization task. The basic finding was extended to children, teens, and adults with dyslexia from familial and clinically-referred samples. Dyslexics showed the same overall pattern of phonology errors and the results were consistent across dyslexia samples, across age groups, and across experimental conditions using word and nonword homophone foils. The dyslexic groups differed from chronological-age matched controls by having elevated false-positive homophone error rates overall, and weaker effects of baseword frequency. Children with dyslexia also made more false-positive errors to spelling control foils. These findings suggest that individuals with dyslexia make use of phonology when making semantic decisions both to word homophone and non-word pseudohomophone foils and that dyslexics lack adequate knowledge of actual word spellings, compared to chronological-age and reading-level matched control participants. [ABSTRACT FROM AUTHOR]

Abstract: We investigated the phonological and surface subtypes of developmental dyslexia in light of competing predictions made by two computational models of single word reading, the Dual-Route Cascaded Model (DRC; Coltheart, Rastle, Perry, Langdon, & Ziegler, 2001) and Harm and Seidenberg’s connectionist model (HS model; Harm & Seidenberg, 1999). The regression-outlier procedure was applied to a large sample to identify children with disproportionately poor phonological coding skills (phonological dyslexia) or disproportionately poor orthographic coding skills (surface dyslexia). Consistent with the predictions of the HS model, children with “pure” phonological dyslexia, who did not have orthographic deficits, had milder phonological impairments than children with “relative” phonological dyslexia, who did have secondary orthographic deficits. In addition, pure cases of dyslexia were more common among older children. Consistent with the predictions of the DRC model, surface dyslexia was not well conceptualized as a reading delay; both phonological and surface dyslexia were associated with patterns of developmental deviance. In addition, some results were problematic for both models. We identified a small number of individuals with severe phonological dyslexia, relatively intact orthographic coding skills, and very poor real word reading. Further, a subset of controls could read normally despite impaired orthographic coding. The findings are discussed in terms of improvements to both models that might help better account for all cases of developmental dyslexia. [Copyright &y& Elsevier]

Background: Reading disability (RD) and attention deficit/hyperactivity disorder (ADHD) are comorbid and genetically correlated, especially the inattentive dimension of ADHD (ADHD-I). However, previous research indicates that RD and ADHD enter into opposite gene by environment (G × E) interactions. Methods: This study used behavioral genetic methods to replicate these opposite G × E interactions in a sample of same-sex monozygotic and dizygotic twin pairs from the Colorado Learning Disabilities Research Center (CLDRC; ) and to test a genetic hypothesis for why these opposite interactions occur. Results: We replicated opposite G × E interactions for RD (bioecological) and ADHD-I (diathesis-stress) with parental education in the same sample of participants. The genetic hypothesis for this opposite pattern of interactions is that only genes specific to each disorder enter into these opposite interactions, not the shared genes underlying their comorbidity. To test this hypothesis, we used single models with an exploratory three-way interaction, in which the G × E interactions for each disorder were moderated by comorbidity. Neither three-way interaction was significant. The heritability of RD did not vary as a function of parental education and ADHD-I. Similarly, the heritability of ADHD-I did not vary as a function of parental education and RD. Conclusions: We documented opposite G × E interactions in RD and ADHD-I in the same overall twin sample, but the explanation for this apparent paradox remains unclear. Examining specific genes and more specific environmental factors may help resolve the paradox. [ABSTRACT FROM AUTHOR]

This study tests a multiple cognitive deficit model of reading disability (RD), attention-deficit/hyperactivity disorder (ADHD), and their comorbidity. A structural equation model (SEM) of multiple cognitive risk factors and symptom outcome variables was constructed. The model included phonological awareness as a unique predictor of RD and response inhibition as a unique predictor of ADHD. Processing speed, naming speed, and verbal working memory were modeled as potential shared cognitive deficits. Model fit indices from the SEM indicated satisfactory fit. Closer inspection of the path weights revealed that processing speed was the only cognitive variable with significant unique relationships to RD and ADHD dimensions, particularly inattention. Moreover, the significant correlation between reading and inattention was reduced to non-significance when processing speed was included in the model, suggesting that processing speed primarily accounted for the phenotypic correlation (or comorbidity) between reading and inattention. This study illustrates the power of a multiple deficit approach to complex developmental disorders and psychopathologies, particularly for exploring comorbidities. The theoretical role of processing speed in the developmental pathways of RD and ADHD and directions for future research are discussed. [ABSTRACT FROM AUTHOR]

Abstract: Purpose: Children with speech sound disorder (SSD) and reading disability (RD) have poor phonological awareness, a problem believed to arise largely from deficits in processing the sensory information in speech, specifically individual acoustic cues. However, such cues are details of acoustic structure. Recent theories suggest that listeners also need to be able to integrate those details to perceive linguistically relevant form. This study examined abilities of children with SSD, RD, and SSD+RD not only to process acoustic cues but also to recover linguistically relevant form from the speech signal. Method: Ten- to 11-year-olds with SSD (n =17), RD (n =16), SSD+RD (n =17), and Controls (n =16) were tested to examine their sensitivity to (1) voice onset times (VOT); (2) spectral structure in fricative-vowel syllables; and (3) vocoded sentences. Results: Children in all groups performed similarly with VOT stimuli, but children with disorders showed delays on other tasks, although the specifics of their performance varied. Conclusion: Children with poor phonemic awareness not only lack sensitivity to acoustic details, but are also less able to recover linguistically relevant forms. This is contrary to one of the main current theories of the relation between spoken and written language development. Learning outcomes: Readers will be able to (1) understand the role speech perception plays in phonological awareness, (2) distinguish between segmental and global structure analysis of speech perception, (3) describe differences and similarities in speech perception among children with speech sound disorder and/or reading disability, and (4) recognize the importance of broadening clinical interventions to focus on recognizing structure at all levels of speech analysis. [Copyright &y& Elsevier]

Purpose: In this study, the authors evaluated literacy outcome in children with histories of speech sound disorder (SSD) who were characterized along 2 dimensions: broader language function and persistence of SSD. In previous studies, authors have demonstrated that each dimension relates to literacy but have not disentangled their effects. Methods: Two groups of children (86 SSD and 37 controls) were recruited at ages 5-6 and were followed longitudinally. The authors report the literacy of children with SSD at ages 7-9, compared with controls and national norms, and relative to language skill and SSD persistence (both measured at age 5-6). Results: The SSD group demonstrated elevated rates of reading disability. Language skill but not SSD persistence predicted later literacy. However, SSD persistence was associated with phonological awareness impairments. Phonological awareness alone predicted literacy outcome less well than a model that also included syntax and nonverbal IQ. Conclusions: Results support previous literature findings that SSD history predicts literacy difficulties and that the association is strongest for SSD + language impairment (LI).Magnitude of phonological impairment alone did not determine literacy outcome, as predicted by the core phonological deficit hypothesis. Instead, consistent with a multiple deficit approach, phonological deficits appeared to interact with other cognitive factors in literacy development. [ABSTRACT FROM AUTHOR]

In this article, we critically review the evidence for overlap among three developmental disorders, namely speech sound disorder (SSD), language impairment (Li), and reading disability (RD), at three levels of analysis: diagnostic, cognitive, and etiological. We find that while overlap exists at all three levels, it varies by comorbidity subtype, and the relations among these three disorders are complex and not fully understood. We evaluate which comorbidity models can be rejected or supported as explanations for why and how these three disorders overlap and what new data are needed to better define their relations. [ABSTRACT FROM AUTHOR]

This review includes 1) an explanation of what neuropsychology is, 2) a brief history of how developmental cognitive neuroscience emerged from earlier neuropsychological approaches to understanding atypical development, 3) three recent examples that illustrate the benefits of this approach, 4) issues and challenges this approach must face, and 5) a forecast for the future of this approach. [ABSTRACT FROM AUTHOR]

This article examines Gene X Environment (G X E) interactions in two comorbid developmental disorders reading disability (RD) and attention-deficit/hyperactivity disorder (ADHD)-as a window on broader issues on G )< E interactions in developmental psychology. The authors first briefly review types of G X E interactions, methods for detecting them, and challenges researchers confront in interpreting such interactions. They then review previous evidence for G X E interactions in RD and ADHD, the directions of which are opposite to each other: bioecological for RD and diathesis stress for ADFLD. Given these results, the authors formulate and test predictions about G X E interactions that would be expected at the favorable end of each symptom dimension (e.g., above-average reading or attention). Consistent with their prediction, the authors found initial evidence for a resilience interaction for above-average reading: higher heritability in the presence of lower parental education. However, they did not find a G X E interaction at the favorable end of the ADHD symptom dimension. The authors conclude with implications for future research. [ABSTRACT FROM AUTHOR]

The majority of children who receive special education services meet criteria for reading disability (RD) or attention-deficit/hyperactivity disorder (ADHD), but additional research is needed to understand the long-term academic outcome of children in these groups. Individuals with RD only ( N = 71), ADHD only ( N = 66), both RD and ADHD ( N = 51), or neither disorder ( N = 118) were identified through the ongoing Colorado Learning Disabilities Research Center twin study and retested 5 years later. Results of the follow-up testing indicated that, in addition to ongoing reading difficulties, individuals with RD exhibited higher rates of academic difficulties, depression, and adolescent-onset conduct disorder. Initial ADHD status was associated with academic and social difficulties and elevated rates of nearly all comorbid disorders 5 years later. The group with comorbid RD and ADHD had more stable reading deficits than the group with RD without ADHD and exhibited greater impairment than groups with either disorder alone on outcome measures of academic functioning and social difficulties. These results suggest that individuals with both RD and ADHD are at increased risk for negative outcomes as adolescents and young adults and that when RD and ADHD co-occur, interventions should be provided for both disorders. [ABSTRACT FROM AUTHOR]

Few studies have investigated the role of gene × environment interactions (G × E) in speech, language, and literacy disorders. Currently, there are two theoretical models, the diathesis–stress model and the bioecological model, that make opposite predictions about the expected direction of G × E, because environmental risk factors may either strengthen or weaken the effect of genes on phenotypes. The purpose of the current study was to test for G × E at two speech sound disorder and reading disability linkage peaks using a sib-pair linkage design and continuous measures of socioeconomic status, home language/literacy environment, and number of ear infections. The interactions were tested using composite speech, language, and preliteracy phenotypes and previously identified linkage peaks on 6p22 and 15q21. Results showed five G × E at both the 6p22 and 15q21 locations across several phenotypes and environmental measures. Four of the five interactions were consistent with the bioecological model of G × E. Each of these four interactions involved environmental measures of the home language/literacy environment. The only interaction that was consistent with the diathesis–stress model was one involving the number of ear infections as the environmental risk variable. The direction of these interactions and possible interpretations are explored in the discussion. [ABSTRACT FROM PUBLISHER]

Numerous studies have examined the etiology of the association between reading difficulties and attention-deficit hyperactivity disorder (ADHD) in school-age children, but little is known about the relation between prereading skills and ADHD behaviors prior to the beginning of formal reading instruction. A population-based sample of 809 pairs of preschool twins completed an extensive battery of prereading measures, and the parent of each twin completed an ADHD rating scale. Phenotypic analyses revealed small but significant correlations between DSM-IV inattention ratings and six prereading composite measures, whereas hyperactivity–impulsivity symptoms were not independently associated with any of the prereading scores. Multivariate twin analyses indicated that virtually all of the phenotypic correlation between inattention and prereading performance is attributable to common genetic influences, consistent with results obtained in studies of older twins. Although additional research is needed to test alternative causal models in children younger than five years old, these results are most consistent with the hypothesis that reading difficulties and inattention symptoms are attributable to common genetic influences. [ABSTRACT FROM AUTHOR]

Abstract: This study tested the segmentation hypothesis of dyslexia by measuring implicit phonological representations in reading-disabled 11- to 13-year-olds. Implicit measures included lexical gating, priming, and syllable similarity tasks designed to reduce metalinguistic demands. Children with dyslexia performed consistently worse than CA and RA controls when more segmental representations were required across all three tasks. Implicit phonological representations were correlated with measures of speech perception, phoneme awareness, and phonological short-term memory, but not rapid automatized naming, and accounted for unique variance in predicting reading ability. Results provide strong support for less mature implicit phonological representations in children with dyslexia. [Copyright &y& Elsevier]

Background: Speech sound disorder (SSD) is a common childhood disorder characterized by developmentally inappropriate errors in speech production that greatly reduce intelligibility. SSD has been found to be associated with later reading disability (RD), and there is also evidence for both a cognitive and etiological overlap between the two disorders. The present study tested whether SSD is linked to replicated risk loci for RD. Method: One hundred and eleven probands with SSD and their 76 siblings were tested with measures of speech, phonological memory (Nonword Repetition -- NWR), and phonological awareness and genotyped for linkage markers on chromosomes 1p36, 6p22, and 15q21. Both single point and multipoint linkage were tested with multiple methods. Results: The speech and NWR phenotypes were linked to the RD loci on chromosomes 6 and 15, with suggestive results for the RD locus on chromosome 1. Conclusions: It now appears that several RD loci are pleiotropic for SSD, extending the findings of Stein et al. (2004) for the RD locus on Chromosome 3. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. 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. 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. These results suggest that a history of SSD and comorbid LI are strong correlates of pre-literacy deficits. [ABSTRACT FROM AUTHOR]

Investigates the etiological relationship between two disorders, dyslexia and reading disability (RD) and phonological disorder (PD). Suggestion that the disorders overlap at symptomatic, cognitive and etiological levels of analysis; Evidence that RD and PD run together in families; Finding that the two disorders are coheritable, indicating that the finding of cofamiliarity of RD and PD is at least partially driven by genetic influences.

The heritable nature of reading disability has been well documented (DeFries & Alarcon, 1996), and possible abnormalities of brain structures have been associated with the disorder (Filipek, 1995). However, the etiology of individual differences in morphological brain measures has not been examined extensively. The purpose of this study was to apply behavioral genetic methods to assess the etiology of individual differences in neuroanatomical structures. Measures of reading performance, cognitive ability, and magnetic resonance imaging scans were obtained from 25 monozygotic (MZ) and 23 same-sex dizygotic (DZ) twin pairs with reading disability, and 9 MZ and 9 DZ control twin pairs participating in the Colorado Learning Disabilities Research Center. Results obtained from multiple regression analyses (DeFries & Fulker, 1985, 1988) of these twin data indicated that individual differences in the size of most cortical and subcortical structures were largely due to heritable influences. Moreover, estimates of heritability did not change appreciably after controlling for IQ and total brain size. [ABSTRACT FROM AUTHOR]

This study used a community sample of 494 twins with a reading disability (223 girls, 271 boys) and 373 twins without a reading disability (189 girls, 184 boys) to assess the relation between reading disability (RD) and attention-deficit/hyperactivity disorder (ADHD). Symptoms of DSM-III and DSM-IV ADHD were classified into symptoms of inattention and symptoms of hyperactivity-impulsivity (H/I). Results indicated that individuals with RD were more likely than individuals without RD to meet criteria for ADHD and that the association between RD and ADHD was stronger for symptoms of inattention than for symptoms of H/I. Parents and teachers reported similar rates of ADHD, suggesting that ADHD symptoms were pervasive across settings and were not solely attributable to academic frustration. Analyses of possible gender differences revealed that RD was significantly associated with inattention in both girls and boys but associated with H/I only in boys. This difference may provide a partial explanation for the discrepancy between the gender ratio obtained in referred (approximately 4 boys to 1 girl) and nonreferred (1.2 to 1.5 boys to 1 girl) samples of individuals with RD. Specifically, the hyperactive and impulsive behaviors exhibited by boys with RD may be more disruptive than the inattentive behaviors exhibited by girls and may therefore precipitate more frequent referrals for clinical attention. [ABSTRACT FROM AUTHOR]

To test the hypothesis that the genetic etiology of reading disability differs as a function of IQ, composite reading performance data from 223 pairs of identical twins and 169 pairs of same-gender fraternal twins in which at least one member of each pair was classified with reading disability were subjected to multiple regression analysis (DeFries & Fulker, 1985, 1988). In the total sample, heritability of the group deficit in reading performance (h[sup 2[sub g]]) was .58 (+/-.08). However, when the basic regression model was fitted separately to data from twin pairs with average Wechsler (1974, 1981) full scale IQ scores below 100 or 100 and above, resulting estimates of h[sup 2[sub g]] were .43 and .72, respectively, a significant difference (p ≤=.03, one-tailed). The results of fitting extended regression models to reading performance and continuous IQ data provide evidence that the genetic etiology of reading disability differs as a linear function of IQ (p ≤=.007, one-tailed). These results suggest that IQ is relevant for the diagnosis of reading disability and that environmental influences may be more salient as a cause of reading difficulties in children with lower IQ scores. [ABSTRACT FROM AUTHOR]

PENNINGTON, BRUCE F.; VAN ORDEN, GUY C.; SMITH, SHELLEY D.; GREEN, PHYLLIS A.; and HAITH, MARSHALL M. Phonological Processing Skills and Deficits in Adult Dyslexics. CHILD DEVELOPMENT, 1990, 61, 1753-1778. This article presents 4 experiments aimed at defining the primary underlying phonological processing deficit(s) in adult dyslexia. 5 phonological processes, all involving spoken language, were studied: phoneme perception, phoneme awareness, lexical retrieval of phonology, articulatory speed, and phonetic coding in verbal short-term memory. 2 differently ascertained adult dyslexic groups, familial dyslexics (n = 15) and clinic dyslexics (n = 15), were the subjects in each experiment. These dyslexic groups were chosen because deficits that persist until adulthood and that are found in differently ascertained dyslexic groups are more likely to be primary. Each dyslexic group was compared to 2 control groups, chronological age (CA) controls who were similar in age and sex, and younger reading age (RA) controls who were similar in reading age and sex. The main finding was a clear deficit in phoneme awareness in both dyslexic groups, with each dyslexic group performing significantly worse than both CA and RA controls. Moreover, performance on the 2 phoneme awareness tasks together uniquely accounted for substantial variance in nonword reading. The clinic but not the familial dyslexics appeared to have an additional deficit in verbal short-term memory. No clear deficits were found in either dyslexic group in phoneme perception, lexical retrieval, or articulatory speed. [ABSTRACT FROM PUBLISHER]

Presents a study which examined genetic hypotheses about the mode of transmission of developmental dyslexia by performing complex segregation analyses. Description of the study's design and setting; Possibility of autosomal dominant transmission of dyslexia; Diagnosis of reading disability; Shortcomings of the Colorado Family Reading Study.

Genetic linkage analysis is a means of localizing genes to specific chromosomal regions. Localization of genes influencing specific reading disability (dyslexia) can lead to characterization of the phenotypic effects of each gene and to early diagnosis of children at risk. Previous studies using the family study LOD score method of linkage analysis have identified two chromosomal regions that may contain genes influencing dyslexia. The present study examines the sib pair method of linkage analysis, which has several advantages over the LOD score method. In particular, the mode of inheritance does not need to be specified and diagnosis of parents is not required, but it is a less powerful technique. Using the same population as the previous studies (with less than 200 sib pairs) and two different means of diagnosis of dyslexia, the sib pair analysis was able to detect the same suggested linkages as the LOD score method, plus a possible third region. This confirms that the sib pair method is an effective means of screening for linkage with reasonable sample sizes. [ABSTRACT FROM AUTHOR]

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 offspring's 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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

This paper reviews what is currently known about the genetics of dyslexia and shows how genetic studies can help clarify which symptoms are primary and which are secondary in dyslexia. On the genetic side, current evidence supports the view that dyslexia is familial, substantially heritable, and heterogeneous in its genetic mechanisms. At least some forms of familial dyslexia appear to be autosomal dominant, with linkage studies supporting both a major locus on chromosome 15 and genetic heterogeneity. On the symptom side, current evidence supports the view that the primary symptom in dyslexia is a deficit in the phonological coding of written language. This primary symptom likewise appears to be heritable. Recent evidence suggests that the heritable precursor to this written language deficit is a spoken language deficit in the skill of phoneme segmentation and awareness. [ABSTRACT FROM AUTHOR]

A pervasive assumption in most accounts of normal reading and spelling development is that phonological coding is important early in development but is subsequently superseded by faster, orthographic coding which bypasses phonology. We call this assumption, which derives from dual process theory, the developmental bypass hypothesis. The present study tests four specific predictions of the developmental bypass hypothesis by comparing dyslexics and none dyslexics from the same families in a cross-sectional design. The four predictions are: 1) That phonological coding skill develops early in normal readers and soon reaches asymptote, whereas orthographic coding skill has a protracted course of development; 2) that the correlation of adult reading or spelling performance with phonological coding skill is considerably less than the correlation with orthographic coding skill; 3) that dyslexics who are mainly deficient in phonological coding skill should be able to bypass this deficit and eventually close the gap in reading and spelling performance; and 4) that the greatest differences between dyslexics and developmental controls on measures of phonological coding skill should be observed early rather than late in development. None of the four predictions of the developmental bypass hypothesis were upheld. Phonological coding skill continued to develop in nondyslexics until adulthood. It accounted for a substantial (32-53 percent) portion of the variance in reading and spelling performance in adult nondyslexics, whereas orthographic coding skill did not account for a statistically reliable portion of this variance. The dyslexics differed little across age in phonological coding skill, but made linear progress in orthographic coding skill, surpassing spelling-age (SA) controls by adulthood. Nonetheless, they did not close the gap in reading and spelling performance. Finally, dyslexics were significantly worse than SA (and Reading Age [RA] controls in phonological coding skill only in adulthood. [ABSTRACT FROM AUTHOR]

Studies the external validity of age-discrepancy and intelligence quotient-discrepancy definitions of reading disability. Similarity between the multifactorial etiology of reading ability and disability; Neurobiological significance of sex ratio and other clinical correlates.

Investigates childhood cognitive deficits in reading disability (RD) and attention-deficit hyperactivity disorder (ADHD) in Colorado. Use of twins in determining performance disability in reading; Analysis of executive functioning factors; Association between RD and ADHD.

Detection thresholds for two visual- and two auditory-processing tasks were obtained for 73 children and young adults who varied broadly in reading ability. A reading-disabled subgroup had significantly higher thresholds than a normal-reading subgroup for the auditory tasks only. When analyzed across the whole group, the auditory tasks and one of the visual tasks, coherent motion detection, were significantly related to word reading. These effects were largely independent of ADHD ratings; however, none of these measures accounted for significant variance in word reading after controlling for full-scale IQ. In contrast, phoneme awareness, rapid naming, and nonword repetition each explained substantial, significant word reading variance after controlling for IQ, suggesting more specific roles for these oral language skills in the development of word reading. [Copyright &y& Elsevier]

Examines the quantitative-trait locus (QTL) for specific language and reading disability on chromosome 6p. Efficacy of multi-point interval-mapping for sin pair QTL analyses; Impact of QTL on different components of reading process; Characterization of the component of QTL.