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.

In children, MNREAD charts provide measurements of reading acuity as reliable as ETDRS chart measurements of distance acuity on a logMAR scale. They also provide highly reliable measurements of the maximum reading speed across all grades, independent of its noticeable increase.

BackgroundAlthough dyslexia is one of the most common neurobehavioral disorders affecting children, prevalence is uncertain and available data are scanty and dated. The objective of this study is to evaluate the prevalence of dyslexia in an unselected school population using clearly defined and rigorous diagnostic criteria and methods.MethodsCross sectional study. We selected a random cluster sample of 94 fourth grade elementary school classes of Friuli Venezia Giulia, a Region of North Eastern Italy. We carried out three consecutive levels of screening: the first two at school and the last at the Neuropsychiatry Unit of a third level Mother and Child Hospital. The main outcome measure was the prevalence of dyslexia, defined as the number of children positive to the third level of screening divided by the total number of children enrolled.ResultsWe recruited 1774 children aged 8–10 years, of which 1528 received parents’ consent to participate. After applying exclusion criteria, 1357 pupils constituted the final working sample. The prevalence of dyslexia in the enrolled population ranged from 3.1% (95% CI 2.2–4.1%) to 3.2% (95% CI 2.4–4.3%) depending on different criteria adopted. In two out of three children with dyslexia the disorder had not been previously diagnosed.ConclusionsThis study shows that dyslexia is largely underestimated in Italy and underlines the need for reliable information on prevalence, in order to better allocate resources both to Health Services and Schools.

Although developmental dyslexia (DD) is frequently associate to a linguistic deficit, the underlying neurobiological cause remains unclear. One prominent vision science hypothesis suggests a specific deficit in magnocellular (M) pathway in DD. However, a recent hypothesis proposes that M-deficits contribute to the etiology of phonological decoding ability (i.e., new word and nonword reading), impairing selectively the attentional orienting process onto letter string. Thus, a specific M-pathway impairment in association with an attentional orienting disorder in DD children with phonological decoding deficit was specifically predicted by this neurobiological hypothesis. In the present study we investigated the M-pathway and attentional orienting in 18 dyslexic (10 with phonological decoding deficit) and in 29 chronological age and IQ matched normally reading children by measuring dynamic stimuli sensibility (i.e., spatial frequency doubling illusion) and the time-course of automatic covert attention (i.e., target detection effect at different SOAs of a non-predictive and peripheral spatial cue), respectively. The results showed a specific deficit of the M-pathway task in dyslexic with phonological decoding deficit. More importantly, the same group of dyslexics with M-deficit presented a sluggish attentional orienting: attentional facilitation was present at longer cue-target SOAs compared with normal readers. These results highlight that a M-deficit linked to a parietal-attentional dysfunction might impair the phonological decoding mechanisms that are critical for reading acquisition