Talcott, J. B. 1 & Valdois, S. 2
1 Aston Brain Centre, Aston University, Birmingham UK
2 Laboratoire de Psychologie et Neurocognition, Université Pierre Mendès-France
Joel B. Talcott
Although there has been significant progress in our understanding of the cognitive architecture that underpins the development of both normal and atypical literacy skills, our knowledge about the nature of developmental dyslexia remains much less advanced. As developmental dyslexia is characterised by a diverse constellation of symptoms, it seems natural to ask whether the underlying risk and protective factors aggregate into subtypes of individuals or not and this is currently an active area of research. To date, this pursuit has been most successful in identifying clusters of individuals with presumed dissociations between specific components of reading, consistent with two theoretical approaches: the dual route model and the double deficit hypotheses. Both models predict the occurrence of discrete subtypes of individuals, with relatively isolated deficits in a single component process and comparatively normal functioning in the other. Each approach has reported subtypes of dyslexia that are largely consistent with its own theoretical perspective. The evidence for these subtypes largely derives from measuring the proportion of individuals who score below some arbitrary threshold on one or both of two theoretically relevant cognitive tasks. However, defined in this way, any continuous bivariate distribution will reveal individuals with single or combined deficits and the proportion in each category that will arise by chance can be estimated through straightforward statistical modelling. Applying these estimates to published data on dyslexia subtypes suggests that the frequencies observed in each group in empirical studies often fail to differ significantly from what would be expected by chance. This provides a powerful challenge to the use of this simple dissociation logic in this context and suggests that stronger evidence is required in order to reify the existence of distinct diagnostic entities from such data.
Evidence for developmental dyslexia subtypes requires that groups of dyslexic children can be identified, each showing a different underlying cognitive disorder and a different neurobiological dysfunction. Thus, relevant subgroups have to be cognitively homogeneous. However, none of the classical reading-based subgroups (phonological vs. surface dyslexia) or the double deficit hypothesis guarantees the homogeneity assumption. In the same way, while cluster analysis may identify statistically reliable subtypes, these subtypes are not necessarily theoretically relevant. Thus even the powerful multivariate method faces with the key problem of distinguishing causal factors from associated ones. Assuming that single-case studies may provide relevant information, we carried out in depth investigation of single cases with no phonological disorder. Such investigation showed evidence for a multiple-element parallel processing disorder --i.e. a visual attention (VA) span disorder-- that was viewed as a potential candidate to account for a second non-phonological subtype of developmental dyslexia. Subsequent group studies revealed that phonological and VA span disorders typically dissociate in the dyslexic population AND are independent predictors of reading performance in both dyslexic and typical readers. The overall findings thus suggest the existence of at least two subgroups of dyslexic children: a phonologically impaired subgroup and a VA span impaired subgroup. Because subgroups have to be defined at the cognitive AND neurobiological level, we explored the neural underpinnings of the VA span disorder. Results suggest that the double dissociation found at the cognitive level is mirrored by a neurobiological dissociation. Whereas the phonological subtype relates to a left hemisphere perisylvian dysfunction, the VA span subtype is associated with a bilateral superior parietal lobule dysfunction.
Evidence for two phonological and VA span subtypes is further supported by the multi-trace memory model which specifies how these two cognitive processes interact to produce skilled reading. Further research is needed to investigate the genetic bases of these two disorders.