ABSTRACT
On paper, clinical categories like dyslexia or specific language impairment (SLI) refer to cognitive disorders in which only language becomes impaired and that can be distinguished from other similar categories at all levels of analysis (phenotypic, cognitive, neurobiological, genetic, etc.). For example, people suffering from dyslexia have difficulties reading texts and spelling words (Lyon et al. 2003). These problems are thought to be caused by the dysfunction of the phonological component of the working memory (Shaywitz et al. 1998). Additionally, the brains of dyslexics show anomalies that are both structural (Galaburda et al. 1985, Deutsch et al. 2005) and functional (Shaywitz et al. 1998, Maisog et al. 2008) and which concern many of the brain areas involved in reading and spelling in the non-affected population (see Démonet et al. 2004 for review). Finally, most of the several candidate genes for dyslexia identified to date regulate axonal growth and neuronal migration in the cortex, plausibly accounting for the structural and functional anomalies attested in the brains of dyslexics (see Benítez-Burraco 2010 for review).
