DEVELOPMENTAL DYSLEXIA, NEURAL TIMING AND HEMISPHERIC LATERALIZATION

Approximately 5% of 8-10-year-olds experience exceptional difficulties learning to read (developmental dyslexia). This usually has a congeni tal basis; it runs in families, and affects 4 times as many boys as gi rls. 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 abili ty 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 hav e lowered nicker and motion sensitivity, and disorder of the magnocell ular layers of the Lateral Geniculate Nucleus can be seen post mortem. Likewise they have lowered sensitivity to changes in frequency and am plitude of sounds, hence impaired discrimination of speech sounds. The se disorders are associated with abnormal hemispheric lateralisation i n these subjects, e.g. dyslexics show reduction or reversal of the usu al left > right asymmetry of the planum temporale. Many of these chara cteristics of impaired magnocellular function and reversed hemispheric asymmetry are found not only in dyslexic children but also in develop mental dysphasics, autistics, high schizotypes and schizophrenics. I w ill speculate therefore that normal magnocellular development promotes normal hemispheric asymmetry and that impaired magnocellular developm ent is responsible for a spectrum of problems associated with impaired hemispheric specialisation, ranging from the mildest, dyslexia, to th e most severe, schizophrenia.