Literacy Maturity and the Magnocellular Theory of Dyslexia: Implications for Clinical Diagnosis

Dyslexia diagnosis suffers from reduced diagnostic power without a diagnostic sign, or a distinguishing characteristic to pinpoint the diagnosis. Many argue that phonological skill provides a diagnostic sign (Ramus et al., 2003), yet not every child with dyslexia shows phonological weakness (Frederickson & Frith, 1998; White et al., 2006). Others argue that deviant magnocellular (m-cell) function may serve as a diagnostic sign (Stein, 2019). However, very few studies on m-cell deviance in dyslexia account for literacy acquisition in their models (Goswami, 2015), and it has been suggested that literacy acquisition may drive m-cell development (Olulade et al., 2013). This study tested the usefulness of m-cells as a diagnostic sign of dyslexia by comparing m-cell function in 8-to 14-year-old children with dyslexia to age-matched peers and younger, reading level-matched peers, accounting for nonverbal ability in a multiple regression model. M-cell function was assessed with a coherent motion task targeting area V5/MT. Results indicate that not all children with dyslexia have deviant m-cell performance in area V5/MT; however, the opposing theory of literacy-driven m-cell development also lacked support. Timed nonword reading appeared a more likely diagnostic sign than m-cell function, and results of an exploratory multiple regression analysis confirmed deviance in timed nonword ability for children with dyslexia, accounting for timed sight word reading and phonological ability. Though typically used to support a phonological-only approach to dyslexia, timed nonword reading has a heavy orthographic component that requires visual input. Given the biological basis of timed nonword reading, the role of m-cells in dyslexia could not be ruled out at this time. Implications for dyslexia diagnosis are discussed, and a cohesive rather than competitive approach to future research on dyslexia’s biological origin is presented.