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Dysfunction of the auditory thalamus in developmental dyslexia

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Díaz,  Begoña
Max Planck Research Group Neural Mechanisms of Human Communication, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Hintz,  Florian
Max Planck Research Group Neural Mechanisms of Human Communication, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Kiebel,  Stefan J.
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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von Kriegstein,  Katharina
Max Planck Research Group Neural Mechanisms of Human Communication, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Citation

Díaz, B., Hintz, F., Kiebel, S. J., & von Kriegstein, K. (2012). Dysfunction of the auditory thalamus in developmental dyslexia. Proceedings of the National Academy of Sciences of the United States of America, 109(34), 13841-13846. doi:10.1073/pnas.1119828109.


Cite as: http://hdl.handle.net/11858/00-001M-0000-000F-C5E1-A
Abstract
Developmental dyslexia, a severe and persistent reading and spelling impairment, is characterized by difficulties in processing speech sounds (i.e., phonemes). Here, we test the hypothesis that these phonological difficulties are associated with a dysfunction of the auditory sensory thalamus, the medial geniculate body (MGB). By using functional MRI, we found that, in dyslexic adults, the MGB responded abnormally when the task required attending to phonemes compared with other speech features. No other structure in the auditory pathway showed distinct functional neural patterns between the two tasks for dyslexic and control participants. Furthermore, MGB activity correlated with dyslexia diagnostic scores, indicating that the task modulation of the MGB is critical for performance in dyslexics. These results suggest that deficits in dyslexia are associated with a failure of the neural mechanism that dynamically tunes MGB according to predictions from cortical areas to optimize speech processing. This view on task-related MGB dysfunction in dyslexics has the potential to reconcile influential theories of dyslexia within a predictive coding framework of brain function.