Cortical thickness abnormalities associated with dyslexia, independent of remediation status

Abstract

Abnormalities in cortical structure are commonly observed in children with dyslexia in key regions of the “reading network.” Whether alteration in cortical features reflects pathology inherent to dyslexia or environmental influence (e.g., impoverished reading experience) remains unclear. To address this question, we compared MRI-derived metrics of cortical thickness (CT), surface area (SA), gray matter volume (GMV), and their lateralization across three different groups of children with a historical diagnosis of dyslexia, who varied in current reading level. We compared three dyslexia subgroups with: (1) persistent reading and spelling impairment; (2) remediated reading impairment (normal reading scores), and (3) remediated reading and spelling impairments (normal reading and spelling scores); and a control group of (4) typically developing children. All groups were matched for age, gender, handedness, and IQ. We hypothesized that the dyslexia group would show cortical abnormalities in regions of the reading network relative to controls, irrespective of remediation status. Such a finding would support that cortical abnormalities are inherent to dyslexia and are not a consequence of abnormal reading experience. Results revealed increased CT of the left fusiform gyrus in the dyslexia group relative to controls. Similarly, the dyslexia group showed CT increase of the right superior temporal gyrus, extending into the planum temporale, which resulted in a rightward CT asymmetry on lateralization indices. There were no group differences in SA, GMV, or their lateralization. These findings held true regardless of remediation status. Each reading level group showed the same “double hit” of atypically increased left fusiform CT and rightward superior temporal CT asymmetry. Thus, findings provide evidence that a developmental history of dyslexia is associated with CT abnormalities, independent of remediation status.

Apparent thinning of visual cortex during childhood is associated with myelination, not pruning

“…as these studies will impact future policies that promote the health and well--being of children. Finally, our data have important ramifications for understanding typical 60 and atypical brain development as well as for clinical conditions implicating myelin and morphology including autism 61 , dyslexia 62 , and multiple sclerosis 63 .…”

Multi-parameter machine learning approach to the neuroanatomical basis of developmental dyslexia

“…Alternative measurements of cortical grey matter anatomical integrity, such as cortical thickness (CT) and surface area (SA) have been used less often for investigating dyslexia [Altarelli et al, 2013;Clark et al, 2014;Frye et al, 2010;Ma et al, 2014]. Here again, the pattern of results is inconsistent.…”

“…Reports vary between lesser [Altarelli et al, 2013;Clark et al, 2014] and greater CT [Ma et al, 2014] in the left fusiform gyrus in dyslexic children, and no CT differences but lower SA in dyslexic adults [Frye et al, 2010]. Other findings include greater CT in the right superior temporal gyrus, planum temporale, middle temporal gyrus, Heschl's gyrus and supramarginal gyrus [Ma et al, 2014]; lesser CT in the left orbitofrontal cortex and in the anterior segment of the superior temporal cortex [Clark et al, 2014], as well as decreased SA in inferior frontal gyrus [Frye et al, 2010]. A recent study [Im et al, 2016] using yet another univariate technique, a graph-based sulcal pattern comparison method, found that the pattern of the sulcal basin area in the left temporo-parietal cortex was atypical in dyslexia.…”

Neurobiological bases of reading disorder Part I: Etiological investigations

“…On the other hand, training-driven normalization in the left OTC has been found at the functional level, including activation during overt single word reading (Heim et al, 2015) and intrinsic functional connectivity at rest (Koyama et al, 2013). This is in contrast to cortical thickness abnormalities in the same region that persist even after intervention (Ma et al, 2015), which suggest a possible causal impairment in the ventral pathway, at the neuroanatomical rather than neurofunctional level.…”