Abstract
An M-pathway deficit has often been associated psychophysically with dyslexia. However there are few physiological studies testing this or attempting to determine the first locus within the visual pathway of any abnormal processing. Thus Magno (M) and parvocellular (P) function was assessed, following Klistorner et al (1997) using second order Wiener kernels of the multi-focal non-patterned visual evoked potential (mfVEP) at short interaction times (sensitive to M) and at longer interaction time (sensitive to P). The subjects included 24 normally reading children (6–12yrs) 14 dyslexics and 3 poor readers with Asperger syndrome. Transient attention was assessed using a custom designed change detection task (requiring parietal activation) and mfVEPs were measured (VERIS system) at luminance contrasts of 24% and 94%. Although the dyslexic children generally showed a ratio of P/M amplitudes similar to those of normal children of similar ages, the mfVEPs of the Asperger group were characterised by short latency larger amplitude more mature M waveforms and a large latency difference (40 msec) between M and P peaks for children of similar age. Change detection was significantly reduced in the dyslexic population compared with normal (Rutkowski et al, 2003) but was normal for the Asperger group.