Developmental dyslexia

Abstract

Developmental dyslexia, or specific reading disability, is a disorder in which children with normal intelligence and sensory abilities show learning deficits for reading. Substantial evidence has established its biological origin and the preponderance of phonological disorders even though important phenotypic variability and comorbidity have been recorded. Diverse theories have been proposed to account for the cognitive and neurological aspects of dyslexia. Findings of genetic studies show that different loci affect specific reading disability although a direct relation has not been established between symptoms and a given genomic locus. In both children and adults with dyslexia, results of neuroimaging studies suggest defective activity and abnormal connectivity between regions crucial for language functions--eg, the left fusiform gyrus for reading--and changes in brain activity associated with performance improvement after various remedial interventions.

Event-related potentials in clinical research: Guidelines for eliciting, recording, and quantifying mismatch negativity, P300, and N400

“…When multiple language skills are assessed, individuals with a developmental language disorder differ substantially from one another in areas of strength and weakness. However, there is no general agreement on the number or nature of distinct disorders or subtypes of developmental language disorder (Bishop, 1997;Démonet et al, 2004;Plante and Beeson, 2007). Thus, ''dyslexia" in one laboratory may be ''specifically language impaired" in another laboratory.…”

Reduced hemispheric asymmetry of the auditory N260m in dyslexia

“…This difference might be explained by varying sample sizes (n= 14 for (Heim et aI., 2003b); n=55 in the present study) and age distributions (8-16 years for (Heim et aI., 2003b); 8-10 years in the present study). A generally high heterogeneity in the phenotype of dyslexia (Demonet, Taylor, & Chaix, 2004;Frith, 2001) might also contribute to differences in sample characteristics. The discrepant findings may well reflect the mixed results characterising the current :MEG literature on clinical populations (Breier et aI., 2003;Helenius, Salmelin, Richardson, Leinonen, & Lyytinen, 2002;Parviainen Helenius, & Salmelin, 2005).…”

ADHD: strategies to unravel its genetic architecture

“…An extension study in a larger sample of 227 ASPs that focused on chromosome 16q13 was able to establish linkage (LOD score 4.2) . A further follow-up investigation extended the original sample of 126 1 UCLA study of 270 sib-pairs Smalley et al, 2002;Ogdie et al, 2003Ogdie et al, , 2004 2 Dutch study of 164 sib-pairr (Bakker et al, 2003) 3 Columbian study of 14 three-generation pedigrees (Arcos-Burgos et al, 2004) 4 For review of genome scans in autism, see Muhle et al (2004) 5 For review of genome scans in dyslexia, see Demonet et al (2004) # Replication of same region ASPs to 270 ASPs and provided linkage analyses of the entire sample (Ogdie et al, 2003). Maximum LOD score (MLS) analysis identified suggestive linkage for 17p11 and four nominal regions with MLS values 11.0, including 5p13, 6q14, 11q25, MLS p 2.98 and 20q13.…”