The International Dyslexia Association defines dyslexia as unexpected problems of neurobiological origin in accuracy and rate of oral reading of single real words, single pseudowords, or text or of written spelling. However, prior research has focused more on the reading than the spelling problems of students with dyslexia. A test battery was administered to 122 children who met inclusion criteria for dyslexia and qualified their families for participation in a family genetics study that has been ongoing for over a decade. Their parents completed the same test battery. Although a past structural equation modeling study of typically developing children identified a significant path from handwriting to composition quality, the current structural equation modeling study identified a significant path from spelling to composition for children and their parents with dyslexia. Graphomotor planning did not contribute uniquely to their composition, showing that writing is not just a motor skill. Students with dyslexia do have a problem in automatic letter writing and naming, which was related to impaired inhibition and verbal fluency, and may explain their spelling problems. Results are discussed in reference to the importance of providing explicit instruction in the phonological, orthographic, and morphological processes of spelling and in composition to students with dyslexia and not only offering accommodation for their writing problems. Keywords dyslexia; writing disability; motor skills; automatic handwriting; spelling; written composition 2 Grant P50 33812-06 to -08 from the National Institute of Child Health and Human Development (NICHD) supported this research.Results were presented at the International Neuropsychological Society Meeting in Dublin, Ireland, July 9, 2005. 3 The authors thank Joan Waiss for assistance in scheduling families, and Allison Brooks, Rebecca Brooksher Pirie, Kate Eschen, Sarah Hellwege, Diana Hoffer, Stephanie King, and Dori Zook for administration of the phenotyping test battery to participants and Jon Organ for assistance in preparing the tables. Most of all they acknowledge the contribution to this research of the families who are affected across generations by dyslexia, including the children and their parents.Correspondence to first author at 322 Miller, Box 353600, University of Washington, Seattle, or vwb@u.washington.edu,. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. The current definition of dyslexia recommended by the International Dyslexia Association is unexpectedly low accuracy and/or rate of oral reading or spelling of ne...

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Dyslexia is a common heterogeneous disorder with a significant genetic component. Multiple studies have replicated the evidence for linkage between variously defined phenotypes of dyslexia and chromosomal regions on 15q21 (DYX1) and 6p22.2 (DYX2). Based on association studies and the possibility for functional significance of several polymorphisms, candidate genes responsible for the observed linkage signal have been proposed-DYX1C1 for 15q21, and KIAA0319 and DCDC2 for 6p22.2. We investigated the evidence for contribution of these candidate genes to dyslexia in our sample of multigenerational families. Our previous quantitative linkage analyses in this dataset provided supportive evidence for linkage of dyslexia to the locus on chromosome 15, but not to the locus on chromosome 6. In the current study, we used probands from 191 families for a case control analysis, and proband-parent trios for family-based TDT analyses. The observation of weak evidence for transmission disequilibrium for one of the two studied polymorphisms in DYX1C1 suggests involvement of this gene in dyslexia in our dataset. We did not find evidence for the association of KIAA0319 or DCDC2 alleles to dyslexia in our sample. We observed a slight tendency for an intronic deletion in DCDC2 to be associated with worse performance on some quantitative measures of dyslexia in the probands in our sample, but not in their parents.

Dyslexia is a common learning disability exhibited as a delay in acquiring reading skills despite adequate intelligence and instruction. Reading single real words (real-word reading, RWR) is especially impaired in many dyslexics. We performed a genome scan, using variance-components (VC) linkage analysis and Bayesian Markov chain Monte Carlo (MCMC) joint segregation and linkage analysis, for three quantitative measures of RWR in 108 multigenerational families, with followup of the strongest signals with parametric LOD score analyses. We used single-word reading efficiency (SWE) to assess speed and accuracy of RWR, and word identification (WID) to assess accuracy alone. Adjusting SWE for WID provided a third measure of RWR efficiency.All three methods of analysis identified a strong linkage signal for SWE on chromosome 13q. Based on multipoint analysis with 13 markers we obtained a MCMC intensity ratio of 53.2 (chromosome-wide p < 0.004), a VC LOD score of 2.29, and a parametric LOD score of 2.94, based on a quantitative-trait model from MCMC segregation analysis. A weaker signal for SWE on chromosome 2q occurred in the same location as a significant linkage peak seen previously in a scan for phonological decoding. MCMC oligogenic segregation analysis identified three models of transmission for WID, which could be assigned to two distinct linkage peaks on chromosomes 12 and 15. Taken together, these results indicate a locus for efficiency and accuracy of RWR on chromosome 13, and a complex model for inheritance of RWR accuracy with loci on chromosomes 12 and 15.

Using a multimodal and multi-informant method for diagnosis, we selected 33 children by teacher and parent nomination for attention and work completion problems that met DSM-IV criteria for attention-deficit/hyperactivity disorder (ADHD). Of the 33 children in this group, 21 participated in the initial intervention, and 12 were placed in an ADHD control group and received the intervention after pre- and posttesting. A similarly selected group of 21 children without difficulties in attention and work completion served as a control group. Each child was assessed on pre- and posttest measures of visual and auditory attention. After an 18-week intervention period that included attention and problem-solving training, all children in the intervention and control groups were retested on visual and auditory tasks. Children in both ADHD groups showed significantly poorer initial performance on the visual attention task. Whereas the ADHD intervention group showed commensurate performance to the nondisabled control group after training, the ADHD control group did not show significant improvement over the same period. Auditory attention was poorer compared to the control group for both ADHD groups initially and improved only for the ADHD intervention group. These findings are discussed as a possible intervention for children with difficulties in strategy selection in a classroom setting.