Reading is a unique cognitive human skill crucial to life in modern societies, but for about 10% of children, learning to read is extremely difficult. These children are affected by developmental dyslexia (DD). Although the most common explanation of DD suggest a specific disorder in auditory and phonological processing, several studies show that also a magnocellular-dorsal (MD) pathway dysfunction could be a core deficit in DD. In this thesis will be investigated the MD functioning on children with and without DD by two case-control studies. The causal relationship between MD dysfunction and reading impairment will be investigated through: (i) two longitudinal studies, in which the attentional skills was tested in pre-reading children, and (ii) five intervention studies in which children with DD was treated with a visual-attentional training (i.e., action video game, AVG). The MD functioning was tested with different tasks that are able to capture different skills driven by MD pathway. In particular, the low spatial frequency, processed by MD pathway, will be investigated through Navon tasks in which is important the global perception of the scene. Another aspect linked to the MD pathway, is the signal-to-noise exclusion in which the target is processed filtering the noise, and this will be investigated through a crowding task and visual and auditory attentional noise exclusion tasks. The findings show that the MD functioning is impaired already at pre-reading stage in future poor readers and that AVG training is able to improve reading speed and attentional skills linked to the MD pathway functioning. For these reason it will be sustain the causal role of MD pathway dysfunction in DD, and the DD as a multifactorial neurodevelopmental disorder.

The magnocellular-dorsal pathway dysfunction in developmental dyslexia: Case-control, longitudinal and intervention studies / Bertoni, Sara. - (2019 Jul 11).

The magnocellular-dorsal pathway dysfunction in developmental dyslexia: Case-control, longitudinal and intervention studies

Bertoni, Sara
2019

Abstract

Reading is a unique cognitive human skill crucial to life in modern societies, but for about 10% of children, learning to read is extremely difficult. These children are affected by developmental dyslexia (DD). Although the most common explanation of DD suggest a specific disorder in auditory and phonological processing, several studies show that also a magnocellular-dorsal (MD) pathway dysfunction could be a core deficit in DD. In this thesis will be investigated the MD functioning on children with and without DD by two case-control studies. The causal relationship between MD dysfunction and reading impairment will be investigated through: (i) two longitudinal studies, in which the attentional skills was tested in pre-reading children, and (ii) five intervention studies in which children with DD was treated with a visual-attentional training (i.e., action video game, AVG). The MD functioning was tested with different tasks that are able to capture different skills driven by MD pathway. In particular, the low spatial frequency, processed by MD pathway, will be investigated through Navon tasks in which is important the global perception of the scene. Another aspect linked to the MD pathway, is the signal-to-noise exclusion in which the target is processed filtering the noise, and this will be investigated through a crowding task and visual and auditory attentional noise exclusion tasks. The findings show that the MD functioning is impaired already at pre-reading stage in future poor readers and that AVG training is able to improve reading speed and attentional skills linked to the MD pathway functioning. For these reason it will be sustain the causal role of MD pathway dysfunction in DD, and the DD as a multifactorial neurodevelopmental disorder.
11-lug-2019
Dyslexia, Magnocellular Pathway, Training, Longitudinal Study, Attention
The magnocellular-dorsal pathway dysfunction in developmental dyslexia: Case-control, longitudinal and intervention studies / Bertoni, Sara. - (2019 Jul 11).
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/3422224
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