Developmental dyslexia, neural timing and hemispheric lateralisation.
Approximately 5% of 8-10-year-olds experience exceptional difficulties learning to read (developmental dyslexia). This usually has a congenital basis; it runs in families, and affects 4 times as many boys as girls. Dyslexics typically show impairment both in phonemic segmentation (the subdivision of speech beyond the natural syllabic level) and in sequencing small visual symbols. Both these skills draw upon the ability of the nervous system to time sensory events precisely. A specific magnocellular cell type which expresses a distinctive surface antigen plays a crucial role in these functions. The development of this cell line is probably congenitally impaired in dyslexics. Visually they have lowered flicker and motion sensitivity, and disorder of the magnocellular layers of the Lateral Geniculate Nucleus can be seen post mortem. Likewise they have lowered sensitivity to changes in frequency and amplitude of sounds, hence impaired discrimination of speech sounds. These disorders are associated with abnormal hemispheric lateralisation in these subjects, e.g. dyslexics show reduction or reversal of the usual left > right asymmetry of the planum temporale. Many of these characteristics of impaired magnocellular function and reversed hemispheric asymmetry are found not only in dyslexic children but also in developmental dysphasics, autistics, high schizotypes and schizophrenics. I will speculate therefore that normal magnocellular development promotes normal hemispheric asymmetry and that impaired magnocellular development is responsible for a spectrum of problems associated with impaired hemispheric specialisation, ranging from the mildest, dyslexia, to the most severe, schizophrenia.