Neurobiology of dyslexia: a reinterpretation of the data
- a Laboratoire de Sciences Cognitives et Psycholinguistique (EHESS/CNRS/ENS), 46 rue d'Ulm, 75230 Paris Cedex 5, France
- b Institute of Cognitive Neuroscience, University College London, 17 Queen Square, London WC1N 3AR, UK
Theories of developmental dyslexia differ on how to best interpret the great variety of symptoms (linguistic, sensory and motor) observed in dyslexic individuals. One approach views dyslexia as a specific phonological deficit, which sometimes co-occurs with a more general sensorimotor syndrome. This article on the neurobiology of dyslexia shows that neurobiological data are indeed consistent with this view, explaining both how a specific phonological deficit might arise, and why a sensorimotor syndrome should be significantly associated with it. This new conceptualisation of the aetiology ofdyslexia could generalize to other neurodevelopmental disorders, and might further explain heterogeneity within each disorder and comorbidity between disorders.
Figures and tables from this article:
- Figure 1. Three causal models of the aetiology of developmental dyslexia. Ovals represent traits at the biological, cognitive and behavioural levels of description; arrows represent causal relationships between traits. Only a subset of all possible behavioural manifestations is represented. (a) Traits and relationships postulated by the phonological theory. (b) Traits and relationships postulated by the magnocellular theory. (c) The proposed model. Solid lines are used for core traits of developmental dyslexia, dashed lines for associated traits that are not necessarily present in each affected individual. Cases of comorbidity with other developmental disorders (e.g. specific language impairment) are not represented. Abbreviations: LGN, lateral geniculate nucleus; MGN, medial geniculate nucleus.
- Figure 2. A molecular layer ectopia in a dyslexic subject. Neurons and glia have escaped into the molecular layer of the cortex, through a breach in the external glial limiting membrane, to form an ectopia (between the two arrows). Scale bar, 250 μm. Micrograph kindly provided by Glenn D. Rosen.
- Figure 3. Neurobiology of developmental dyslexia. (a) Overall distribution of cortical ectopias observed across different dyslexic subjects (kindly provided by Glenn D. Rosen). (b) Brain areas activated in oral language tasks and exhibiting structural differences between dyslexics and controls. Areas in orange are supported by one published study, areas in red by more than one. Reproduced, with permission of Sage Publications, Inc., from Ref. [15]. (c) Brain areas activated during performance of the main phonological skills impaired in dyslexia: phonological awareness (yellow), rapid serial naming (red) and verbal short-term memory (blue). Reproduced, with permission, from Ref. [39].
No comments:
Post a Comment