Altered Structural Connectivity of the Left Visual Thalamus in Developmental Dyslexia

Abstract

Developmental dyslexia is a highly prevalent reading disorder affecting about 5%–10% of children [1]. It is characterized by slow and/or inaccurate word recognition skills as well as by poor spelling and decoding abilities [2]. Partly due to technical challenges with investigating subcortical sensory structures, current research on dyslexia in humans by and large focuses on the cerebral cortex [3–7]. These studies found that dyslexia is typically associated with functional and structural alterations of a distributed left-hemispheric cerebral cortex network (e.g., [8, 9]). However, findings from animal models and post mortem studies in humans suggest that dyslexia might also be associated with structural alterations in subcortical sensory pathways [10–14] (reviewed in [7]). Whether these alterations also exist in dyslexia in vivo and how they relate to dyslexia symptoms is currently unknown. Here, we used ultra-high-resolution structural magnetic resonance imaging (MRI), diffusion MRI, and probabilistic tractography to investigate the structural connections of the visual sensory pathway in dyslexia in vivo. We discovered that individuals with dyslexia have reduced structural connections in the direct pathway between the left visual thalamus (lateral geniculate nucleus [LGN]) and left middle temporal area V5/MT, but not between the left LGN and left primary visual cortex. In addition, left V5/MT-LGN connectivity strength correlated with rapid naming abilities—a key deficit in dyslexia [15]. These findings provide the first evidence of specific structural alterations in the connections between the sensory thalamus and cortex in developmental dyslexia. The results challenge current standard models and provide novel evidence for the importance of cortico-thalamic interactions in explaining dyslexia. Müller-Axt et al. show that dyslexics have reduced connections in the direct pathway between the left visual thalamus and cortical area V5/MT. The strength of this pathway predicted a key dyslexia symptom, thereby challenging current dyslexia models and stressing the importance of interactions between cortex and sensory thalamus for cognition.