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Research Support, Non-U.S. Gov't
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A case study of developmental phonological dyslexia: Is the attentional deficit in the perception of rapid stimuli sequences amodal?

The attentional blink (AB) refers to a decrease in accuracy that occurs when participants are required to detect the second of two rapidly sequential targets displayed randomly in a stream of distracters. Dyslexic individuals have been shown to exhibit a prolonged AB in the visual modality, interpreted as evidence of sluggish attentional shifting (SAS). However, the amodal SAS theory predicts that the disorder should further extend to the auditory modality, then resulting in a phonological disorder as typically found in developmental dyslexia. Otherwise, it has been demonstrated that a visual attention (VA) span deficit contributes to the poor reading outcome of dyslexic individuals, independently of their phonological skills. The present study assesses the amodality assumption of the SAS theory together with questioning its relation with the VA span deficit. For this purpose, visual and auditory ABs were explored in a well compensated young adult, LL, who exhibits a pure phonological dyslexia characterised by poor pseudo-word processing and poor phonological skills but preserved VA span. The investigation revealed two different kinds of deficits in LL. Her AB was prolonged and marginally deeper in the visual modality whereas a primarily deeper in amplitude and a subtle prolonged AB was found in the auditory modality. The atypical performance patterns of LL in both modalities suggest that her perceptual attention disorder is amodal as predicted by the SAS theory. This amodal disorder was here reported in a dyslexic participant with a phonological disorder, well in accordance with the hypothesis that sluggish auditory attention shifting contributes to difficulties in phoneme awareness and literacy acquisition. Furthermore, prolonged VA blink was observed in the absence of VA span disorder, thus suggesting that visual attentional shifting and VA span might be distinct mechanisms, contributing independently to reading acquisition and developmental dyslexia.

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