Brain activity patterns of phonemic representations are atypical in beginning readers with family risk for dyslexia

Abstract

There is an ongoing debate whether phonological deficits in dyslexics should be attributed to (a) less specified representations of speech sounds, like suggested by studies in young children with a familial risk for dyslexia, or (b) to an impaired access to these phonemic representations, as suggested by studies in adults with dyslexia. These conflicting findings are rooted in between study differences in sample characteristics and/or testing techniques. The current study uses the same multivariate functional MRI (fMRI) approach as previously used in adults with dyslexia to investigate phonemic representations in 30 beginning readers with a familial risk and 24 beginning readers without a familial risk of dyslexia, of whom 20 were later retrospectively classified as dyslexic. Based on fMRI response patterns evoked by listening to different utterances of /bA/ and /dA/ sounds, multivoxel analyses indicate that the underlying activation patterns of the two phonemes were distinct in children with a low family risk but not in children with high family risk. However, no group differences were observed between children that were later classified as typical versus dyslexic readers, regardless of their family risk status, indicating that poor phonemic representations constitute a risk for dyslexia but are not sufficient to result in reading problems. We hypothesize that poor phonemic representations are trait (family risk) and not state (dyslexia) dependent, and that representational deficits only lead to reading difficulties when they are present in conjunction with other neuroanatomical or—functional deficits.

A universal reading network and its modulation by writing system and reading ability in French and Chinese children

“…In our data, only French poor readers had a significantly lower activation relative to their controls at this location, but in both languages, poor readers exhibited an unstable activation pattern across fMRI runs, suggesting fragile phonetic representations evoked by written stimuli. In agreement with this interpretation, Vandermosten et al, 2020 also observed disrupted phonological representation in a multivariate pattern analysis but not in the univariate activation analysis in beginning readers with a family risk for dyslexia. Again, because this site is also under-activated during spoken language processing in illiterates and in preliterate children compared to adult and children readers ( Dehaene et al, 2010 ) we cannot ascertain whether its anomalous activation is a cause or a consequence of the reading disability.…”

Letter fluency in 7-8-year-old children is related to the anterior, but not posterior, ventral occipito-temporal cortex during an auditory phonological task

“…The left superior temporal gyrus is a region that is reliably engaged during auditory phonological awareness tasks (e.g. Boets et al, 2013 ; Leonard and Chang, 2014 ; Weiss et al, 2018 ; Vandermosten et al, 2020 ; Wang et al, 2020 ). Therefore, it is possible that 7- to 8-year-old children rely more on their refined phonological representations in the left superior temporal gyrus to solve small grain size problems.…”

Putative protective neural mechanisms in prereaders with a family history of dyslexia who subsequently develop typical reading skills

“…Neural alterations in this region have previously been associated with dyslexia (e.g., Peterson & Pennington, ; Richlan et al, ; Shaywitz & Shaywitz, ) as well as familial risk (e.g., Im et al, ; Raschle et al, , ; Raschle et al, ). Recent effort has been made to disentangle these two effects by comparing FHD+ good and/or poor readers with controls (Hakvoort, van der Leij, Maurits, Maassen, & van Zuijen, ; Vanderauwera, Wouters, Vandermosten, & Ghesquière, ; Vandermosten et al, ). Atypical brain responses for speech and phonological processing were observed in bilateral superior temporal regions in both good and poor readers with a family history when compared to controls, indicating an effect of familial risk (Vandermosten et al, ).…”

“…Second, a small group of FHD+Impaired children ( n = 12) were included in the current analyses, limiting the result generalizability. However, it should be noted that the primary analyses have been devoted to characterizing the atypical neural mechanisms underlying reading development in FHD+Typical compared to FHD−Typical children ( n = 60), which few studies have investigated (however, see Vandermosten et al, ). Future studies with a large sample are needed to determine the exact developmental timelines of compensatory/protective mechanisms that support literacy acquisition in FHD+ children.…”