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Magnocellular-dorsal pathway and sub-lexical route in developmental dyslexia
Although developmental dyslexia (DD) is frequently associate with a phonological deficit, the underlying neurobiological cause remains undetermined. Recently, a new model, called “temporal sampling framework” (TSF), provided an innovative prospect in the DD study. TSF suggests that deficits in sylla...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4068287/ https://www.ncbi.nlm.nih.gov/pubmed/25009484 http://dx.doi.org/10.3389/fnhum.2014.00460 |
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author | Gori, Simone Cecchini, Paolo Bigoni, Anna Molteni, Massimo Facoetti, Andrea |
author_facet | Gori, Simone Cecchini, Paolo Bigoni, Anna Molteni, Massimo Facoetti, Andrea |
author_sort | Gori, Simone |
collection | PubMed |
description | Although developmental dyslexia (DD) is frequently associate with a phonological deficit, the underlying neurobiological cause remains undetermined. Recently, a new model, called “temporal sampling framework” (TSF), provided an innovative prospect in the DD study. TSF suggests that deficits in syllabic perception at a specific temporal frequencies are the critical basis for the poor reading performance in DD. This approach was presented as a possible neurobiological substrate of the phonological deficit of DD but the TSF can also easily be applied to the visual modality deficits. The deficit in the magnocellular-dorsal (M-D) pathway - often found in individuals with DD - fits well with a temporal oscillatory deficit specifically related to this visual pathway. This study investigated the visual M-D and parvocellular-ventral (P-V) pathways in dyslexic and in chronological age and IQ-matched normally reading children by measuring temporal (frequency doubling illusion) and static stimuli sensitivity, respectively. A specific deficit in M-D temporal oscillation was found. Importantly, the M-D deficit was selectively shown in poor phonological decoders. M-D deficit appears to be frequent because 75% of poor pseudo-word readers were at least 1 SD below the mean of the controls. Finally, a replication study by using a new group of poor phonological decoders and reading level controls suggested a crucial role of M-D deficit in DD. These results showed that a M-D deficit might impair the sub-lexical mechanisms that are critical for reading development. The possible link between these findings and TSF is discussed. |
format | Online Article Text |
id | pubmed-4068287 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-40682872014-07-09 Magnocellular-dorsal pathway and sub-lexical route in developmental dyslexia Gori, Simone Cecchini, Paolo Bigoni, Anna Molteni, Massimo Facoetti, Andrea Front Hum Neurosci Neuroscience Although developmental dyslexia (DD) is frequently associate with a phonological deficit, the underlying neurobiological cause remains undetermined. Recently, a new model, called “temporal sampling framework” (TSF), provided an innovative prospect in the DD study. TSF suggests that deficits in syllabic perception at a specific temporal frequencies are the critical basis for the poor reading performance in DD. This approach was presented as a possible neurobiological substrate of the phonological deficit of DD but the TSF can also easily be applied to the visual modality deficits. The deficit in the magnocellular-dorsal (M-D) pathway - often found in individuals with DD - fits well with a temporal oscillatory deficit specifically related to this visual pathway. This study investigated the visual M-D and parvocellular-ventral (P-V) pathways in dyslexic and in chronological age and IQ-matched normally reading children by measuring temporal (frequency doubling illusion) and static stimuli sensitivity, respectively. A specific deficit in M-D temporal oscillation was found. Importantly, the M-D deficit was selectively shown in poor phonological decoders. M-D deficit appears to be frequent because 75% of poor pseudo-word readers were at least 1 SD below the mean of the controls. Finally, a replication study by using a new group of poor phonological decoders and reading level controls suggested a crucial role of M-D deficit in DD. These results showed that a M-D deficit might impair the sub-lexical mechanisms that are critical for reading development. The possible link between these findings and TSF is discussed. Frontiers Media S.A. 2014-06-24 /pmc/articles/PMC4068287/ /pubmed/25009484 http://dx.doi.org/10.3389/fnhum.2014.00460 Text en Copyright © 2014 Gori, Cecchini, Bigoni, Molteni and Facoetti. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Gori, Simone Cecchini, Paolo Bigoni, Anna Molteni, Massimo Facoetti, Andrea Magnocellular-dorsal pathway and sub-lexical route in developmental dyslexia |
title | Magnocellular-dorsal pathway and sub-lexical route in developmental dyslexia |
title_full | Magnocellular-dorsal pathway and sub-lexical route in developmental dyslexia |
title_fullStr | Magnocellular-dorsal pathway and sub-lexical route in developmental dyslexia |
title_full_unstemmed | Magnocellular-dorsal pathway and sub-lexical route in developmental dyslexia |
title_short | Magnocellular-dorsal pathway and sub-lexical route in developmental dyslexia |
title_sort | magnocellular-dorsal pathway and sub-lexical route in developmental dyslexia |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4068287/ https://www.ncbi.nlm.nih.gov/pubmed/25009484 http://dx.doi.org/10.3389/fnhum.2014.00460 |
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