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Dyslexia is characterized by differences in intracortical myelination, but not cortical folding patterns, in the superior temporal plane
Poster Session E, Friday, October 2, 11:00 am - 1:00 pm, Wangari Maathai
Yinuo Liu1, Jamie A. Chin1, Tyler K. Perrachione1; 1Boston University
Developmental dyslexia is a reading disorder characterized by phonological processing deficits evident in both behavioral and neurobiological studies (Ramus & Szenkovits, 2008; Snowling, 1998). It has been proposed that atypical structural features of the auditory cortex may contribute to these deficits (Galaburda, 1989). Prior research has examined whether various macroanatomical features of the auditory cortex (such as cortical folding patterns, surface area, thickness, or volume) differ in dyslexia, but results have been inconsistent across studies. Genetic evidence suggests that neuroanatomical differences in dyslexia might occur at a finer microstructural scale, potentially stemming from disrupted neural migration (Gabel et al., 2010). In this study, we investigated two hypotheses of auditory cortical structural differences in dyslexia, namely that dyslexia is associated with differences in: (i) patterns of macrostructural cortical folding in auditory cortex (Leonard et al., 2001), and/or (ii) microstructural features associated with intracortical myelination (Skeide et al., 2018). Structural MRI brain scans were obtained from N=118 adults (63/55 control/dyslexia). Cortical folding patterns were analyzed using cortical surface reconstructions from T1w volumes (n=63/55). Cortical microstructure was examined in unique subsets of the full sample, using either the T1w/T2w ratio in n=50 (25/25) (Glasser & Van Essen, 2011) or R1 relaxometry in n=55 (30/25) (Sigalovsky et al., 2006). Manual labeling of classical Heschl’s gyrus (HG) morphotypes revealed no difference in the likelihood of finding a single HG, common-stem duplication, or complete posterior duplication between groups (chi-squared = 0.342, p = 0.843). Unsupervised, data-driven clustering of the continuous local curvature revealed four distinctive folding patterns in the superior temporal plane, but the prevalence of these morphotypes also did not differ between control and dyslexic brains (chi-squared = 2.82, p = 0.420). In contrast, microstructural analyses showed robust group differences in signal related to intracortical myelin within the superior temporal plane, with significant hypermyelination in dyslexia relative to controls, as measured by both the T1w/T2w ratio (t = 3.07, p = 0.003) and R1 relaxometry (t = 2.09, p = 0.039). These findings indicate that macroanatomical differences in cortical folding, including the prevalence of HG duplications, are not a distinguishing characteristic of the brain in developmental dyslexia. However, auditory cortical hypermyelination was found in two independent samples of dyslexia based on two separate MRI signal contrasts, suggesting that differences in the auditory cortical microarchitecture may underlie functional neurocomputational differences in dyslexia (Hancock et al., 2017; Perrachione et al., 2016) related to the phonological processing deficits and difficulty developing fluent reading skills.
Topic Areas: Disorders: Developmental,