Changing concepts of dyslexia: nature, treatment and comorbidity

Abstract

This topic for this the first Virtual Issue of JCPP was prompted by a recent independent review, Identifying and teaching children and young people with dyslexia and literacy difficulties (Rose, 2009). This review drew on a large evidence-base and took as its working definition that dyslexia is a disorder primarily affecting reading and spelling development, usually associated with impairments of phonological processing, verbal processing speed and verbal short-term memory. It also acknowledged that dyslexia is often accompanied by other features that affect educational attainment (comorbidities), though these are not themselves characteristics of dyslexia. The papers selected for this Virtual Issue have been chosen to reflect the evolution of this view of dyslexia, which can be traced from the landmark Isle of Wight study differentiating specific from general reading difficulties, reported in the journal in 1975 by Rutter and Yule, through the now classic argument of Stanovich (1994) that questioned the utility of the ‘discrepancy definition’ of dyslexia, to the contemporary view of dyslexia as a phonological deficit (Vellutino, Fletcher, Snowling, & Scanlon, 2004). Against this backdrop, a set of papers is presented, each of which highlights that ‘dyslexia’ is not a disorder with clear-cut boundaries or with a single cause. Three papers in the selection address the overlap between reading and language impairment: McArthur, Hogben, Edwards, Heath, and Mengler (2000) report that some 55% of children with specific reading disability (SRD) have oral language difficulties while 51% of children with specific language impairment (SLI) have SRD. However, the risk of SRD depends upon the nature of the language impairment: Raitano, Pennington, Tunick, Boada, and Shriberg (2004) showed that the pre-literacy outcomes of children with pre-school speech impairment (speech sound disorder; SSD) were relatively good unless their speech difficulties were persistent or they had broader language difficulties. The finding of a relatively low risk of reading impairment in children with a history of pure speech impairment is reminiscent of earlier work by Bishop and Adams reported in the journal in 1990, which also showed that specific difficulties with reading comprehension were more common among children with SLI than the pervasive deficits in word-level decoding characteristic of dyslexia. What of children learning to read in languages other than English? It might be supposed that the risk of dyslexia would be less in languages that have more transparent writing systems with fewer irregularities, or in which there are fewer phonological demands because mappings are not at the level of the phoneme (as in alphabetic systems) but involve large units such as syllables or morphemes (e.g., in Chinese). However, Puolakanaho et al. (2007) reported findings from a study of children at family risk of dyslexia in the highly regular Finnish orthography, showing that 36% of ‘at-risk’ children are classified as reading disabled at 8.09 years, a figure comparable to that for children learning to read in English. This study also showed that it was possible, with an acceptable degree of accuracy, to use a small set of measures to predict, as early as 3.5 years, who would develop reading problems. These were letter knowledge, rapid naming (a measure of phonological skill) and family-risk status. Extending the method of a family-risk prospective study to Cantonese, McBride-Chang et al. (2008) found that in the second year of kindergarten (4–5 years), children at family risk were already lagging behind their peers in learning to read Chinese characters and their difficulties were associated with impairments in tone detection (a measure of phonological skill) and in morphological awareness. Language delayed children who also experienced reading difficulties were characterised by a wider range of cognitive and linguistic impairments including these deficits. The increased risk of reading difficulties in children from ‘at-risk’ families is suggestive of a genetic etiology, but since families share environments as well as genes, dyslexia could in principle be the outcome of environmental factors associated with low literacy. Stevenson and Fredman (1990) reported data from a twin study showing that 32% of the variance in reading was accounted for by IQ and social factors including mother’s educational level, family size, housing and social circumstances and some aspects of emotional atmosphere at home. However, when IQ was controlled, only two environmental factors had a significant effect on individual differences in reading; these were family size (a general environmental effect) and maternal criticism (a specific environmental effect that might actually be a consequence of a child’s reading failure). This paper also makes clear that even in propitious circumstances and when literacy instruction is good, some children will still experience reading difficulties. Consistent with this, Kovas et al. (2007), using data from the Twins Early Development Study, showed that reading disability is moderately heritable; further, there was some 33% overlap between reading disability and mathematics disability. While much of this overlap was due to shared genetic factors (generalist genes), there were also genetic influences specific to reading and specific to mathematics. Based on past research, a reasonable hypothesis is that the comorbidity of reading and mathematics disability is due to shared verbal deficits (affecting the development of arithmetic competence) and, as intimated above, the comorbidity of dyslexia and SLI is likely due to shared phonological deficits. As further papers in this issue illustrate, dyslexia also co-occurs with two quite distinct disorders, attention deficit/hyperactivity disorder (ADHD) (Bental & Tirosh, 2007) and developmental coordination disorder (Rochelle & Talcott, 2006), and is associated with a range of other conditions affecting mental health (Carroll, Maughan, Goodman, & Meltzer, 2005). Given knowledge of the nature and characteristics of dyslexia, an ongoing challenge for practitioners who identify dyslexia is the implementation of intervention programmes. Recognising the comorbidity of dyslexia and ADHD, Gittelman and Feingold (1983) were amongst the first to conduct an early controlled trial to evaluate the efficacy of an 18-week phonics intervention as a treatment for poor readers; in a companion paper in the same volume, they evaluated the impact of medication for ADHD on educational outcome. The findings were intriguing; the phonics intervention was effective in promoting reading (but not spelling or arithmetic) whereas the medication (methylphenidate) had an impact on arithmetic but not on reading, hinting perhaps at the greater role of executive processes in arithmetic skill. More recently, Hatcher et al. (2006) showed that a 10-week intervention, combining training in oral phoneme awareness and structured book reading plus activities ‘linking’ the two skills, could be delivered by trained teaching assistants to increase the reading skills of poor readers in Year 1. Extending this work to younger children who enter school with poor speech and language, Bowyer-Crane et al. (2008) showed that the intervention was effective in accelerating reading progress, compared with that of a treated control group who received oral language intervention. A further positive finding was that the oral language programme successfully boosted vocabulary and expressive grammar. The science of dyslexia is well advanced and theory can be used to guide the design of intervention approaches. The papers selected here illustrate the range of research methodologies that have been fruitful to the field and convergent evidence now presents a strong rationale for considering dyslexia as the behavioural outcome of a number of different developmental pathways, mediated by a phonological deficit. Omissions from the issue include important findings from longitudinal studies of epidemiological samples (e.g., Fergusson & Lynskey, 1997) and papers representing molecular genetic (Gayán et al., 2005) and neuroscientific (Eliez et al., 2000) approaches. * indicates papers cited above but not included in the Virtual Issue selection