Multisensory deficits in dyslexia may result from a locus coeruleus attentional network dysfunction.

A fundamental educational requirement of beginning reading is to learn, access, and rapidly process associations between novel visuospatial symbols and their phonological representations in speech. Children with difficulties in such cross-modal integration are often divided into dyslexia subtypes, based on whether their primary problem is with the written or spoken component of decoding. The present review suggests that starting in infancy, perceptions of audiovisual speech are integrated by mutual oscillatory phase-resetting between sensory cortices, and throughout development visual and auditory experiences are coupled into unified perceptions. Entirely separate subtypes are incompatible with this view. Visual or auditory deficits will invariably affect processing to some degree in both domains. It is suggested that poor auditory/visual integration may be diagnostic for both forms of dyslexia, stemming from an encoding weakness in the early cross-sensory binding of audiovisual speech. The review presents a model of dyslexia as a dysfunction of the large-scale ventral and dorsal attention networks controlling such binding. Excessive glutamatergic neuronal excitability of the attention networks by the Locus coeruleus-norepinephrine system may interfere with multisensory integration, with deleterious effects on the acquisition of reading by degrading graphene/phoneme conversion.