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Anomalous gray matter patterns in specific reading comprehension deficit are independent of dyslexia

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Abstract

Specific reading comprehension deficit (SRCD) affects up to 10 % of all children. SRCD is distinct from dyslexia (DYS) in that individuals with SRCD show poor comprehension despite adequate decoding skills. Despite its prevalence and considerable behavioral research, there is not yet a unified cognitive profile of SRCD. While its neuroanatomical basis is unknown, SRCD could be anomalous in regions subserving their commonly reported cognitive weaknesses in semantic processing or executive function. Here we investigated, for the first time, patterns of gray matter volume difference in SRCD as compared to DYS and typical developing (TD) adolescent readers (N = 41). A linear support vector machine algorithm was applied to whole brain gray matter volumes generated through voxel-based morphometry. As expected, DYS differed significantly from TD in a pattern that included features from left fusiform and supramarginal gyri (DYS vs. TD: 80.0 %, p < 0.01). SRCD was well differentiated not only from TD (92.5 %, p < 0.001) but also from DYS (88.0 %, p < 0.001). Of particular interest were findings of reduced gray matter volume in right frontal areas that were also supported by univariate analysis. These areas are thought to subserve executive processes relevant for reading, such as monitoring and manipulating mental representations. Thus, preliminary analyses suggest that SRCD readers possess a distinct neural profile compared to both TD and DYS readers and that these differences might be linked to domain-general abilities. This work provides a foundation for further investigation into variants of reading disability beyond DYS.

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Acknowledgments

This research was supported by NIH grants R01 HD 044073, R01 HD 046130, P30 HD 015052, T32 MH 064913, P41 RR 15241, and CTSA RR 024975 VU.

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Correspondence to Laurie Cutting.

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Bailey, S., Hoeft, F., Aboud, K. et al. Anomalous gray matter patterns in specific reading comprehension deficit are independent of dyslexia. Ann. of Dyslexia 66, 256–274 (2016). https://doi.org/10.1007/s11881-015-0114-y

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