Visual evoked potentials were measured with scalp electrodes in eight reading-disabled children aged 8 to 11 years and compared to a control group of 13 age-matched normal readers at the School of Optometry, University of Missouri, St Louis. Using a steady background and a low-spatial-frequency target (0.5 cycle/degree visual angle), the latencies of the early components (N1 and P1) of the VER were longer and the amplitude of the subsequent (P1-N2) component was smaller in the reading-disabled than in normal readers. A flickering background increased the latency and reduced the amplitude of the early components of the VER in normal readers, whereas in reading-disabled children only the amplitude was affected. These differences were most likely due to a sensory deficit and slowed response in the magnicellular visual pathway of reading-disabled children. [1]

COMMENT. These findings are supported by previous anatomical and electrophysiological studies that have demonstrated a defective magnicellular visual pathway in dyslexic subjects. A cause-and-effect relation between these slowed visual responses and the reading disability remains to be determined.