Disturbi dell'attenzione selettiva nella dislessia evolutiva: evidenze comportamentali, correlati neurobiologici, neurofisiologici e genetici

Reading acquisition requires not only adequate auditory-phonological skills, but also appropriate visuo-perceptual abilities. Some studies have shown that selective attention (SA) specifically affects these abilities. Although children and adults with developmental dyslexia (DD, neurodevelopmental reading deficit) show a phonological deficit, there are a number of theories supporting a non-linguistic sensory mechanisms (Dorsal-Magnocellular pathway, D-M). The non-linguistic deficit might in principal affect a general efficient processing of perceptual stimuli when spatial and temporal signal interference are induced by near noise. Some studies have shown that in individuals with DD, the deficit in reading is significantly affected by a sub-lexical damage. It is widely assumed that the sub-lexical route requires a primary graphemic parsing process (GP; i.e., the visual segmentation of a grapheme string into its constituent graphemes) provided by SA, in addition to phonological processing, memory and grapheme-phoneme correspondences. Our studies attempted to investigate whether SA deficit, probably arised from a D-M dysfunction, could certainly have important consequences for normal reading developmental. SA deficit could selectively affect the rapid GP process necessary for an efficient phonological decoding. Precisely, a selective GP deficit might be due to a sluggish shifting of spatial (i.e., orienting and focusing processes) and temporal (i.e., engagement and disengagement processes) selective visual attention, which is a critical cognitive mechanism to support the perceptual signal processing and the noise exclusion induced by near letters. The aim of this study is to investigate the potential neurobiologcal (i.e., D-M pathway), neurophysiological (i.e., early sensory modulation from posterior parietal cortex to occipital area) and molecular (i.e., cholinergic-nicotinic receptors) basis of the SA deficit in children with DD. Our psychophysical and behavioral results coherently show that a specific spatial and temporal SA deficit, preventing an efficient GP (lead to all subsequent spelling-to-sound conversion processes), is specifically linked to a selective sub-lexical route damage (Experiments 1-6b). In dyslexics impaired in nonword reading (sub-lexical damage) the SA deficit might be linked to a neurodevelopmental deficit at D-M pathway (i.e., lower contrast sensitivity at frequency doubling illusion; Experiment 7a). In addition, an AS deficit seems to affect the signal discrimination ability and the perceptual lateral noise exclusion (Experiment 7b). Importantly, the study of lateral masking and text reading abilities confirms the potential predictive relation between spatial SA and the GP deficit in DD (Experiment 7c). Moreover, the results of visual event-related potential (ERP) study (Experiment 8) show a neurophysiological evidence of a sluggish shifting of visuo-spatial SA in dyslexics with a sub-lexical damage. Precisely, the facilitatory effect of visuo-spatial attention induced by a peripheral cue on the P1 (a early ERP of visual processing) is not present in dyslexics with a sub-lexical damage. Finally, the genetic study (Experiment 9) show that cholinergic-nicotinic receptors (i.e., polymorphism rs3827020 T/C, gene CHRNA4), affecting the intra-parietal lobe activity, might be linked to the visuo-spatial AS deficit and the specific reading deficit in DD. In sum, our results provide psychophysics and behavioral evidences of spatial and temporal SA deficit in children with DD who are impaired in nonword reading. This deficit could be the result of a neurodevelopmental dysfunction of D-M pathway. Moreover, results from the lateral masking study suggest the possible causal relation between the spatial SA deficit and the specific phonological decoding damage, potentially affected by the GP process, which is requisite for the grapheme-phoneme mapping. Finally, we provide neurophysiological (P1 component) and molecular (cholinergic-nicotinic receptors) evidences that the sluggish of visuo-spatial SA might affect the efficiency of sub-lexical route, necessary to learn to read.