There is very little agreement about why so many otherwise intelligent children experience such difficulty learning to read. Up to 10% of children fail to learn to read at the level expected of their age and other cognitive abilities. Some people still believe that their problems are purely linguistic, due to inheriting or acquiring a defective linguistic processor. Others take the view that difficulty with learning to read derives from more basic deficiencies in processing the sensory inputs that are required for reading. According to this view literacy problems are caused by fundamental differences in sensory processing between the brains of good and bad readers, so that in addition to their literacy problems there are many other sensory, motor and cognitive differences to be found in poor readers because the development of the whole brain is disordered. In our laboratory we take the latter position. We study the neurophysiological processes which underlie reading; hence we view reading problems as having a neurodevelopmental basis. In this chapter therefore, I will discuss how normal reading depends on the quality of its sensory input; it absolutely requires both a highly sensitive visual magnocellular system to acquire good orthographic skills and a sensitive auditory transient system to develop the ability to parse the phonological structure of words. Then I will speculate about the genetic and immunological mechanisms that may be responsible for the wide variety of abnormalities that are seen in developmental dyslexics. My overall conclusion will be that reading difficulties are neither specific to reading nor exclusively linguistically based, but a consequence of mildly impaired development of a particular kind of neurons in the brain, magnocellular neurons, so that dyslexia has widespread manifestations, which are not at all confined to reading (Stein Walsh, 1997; Stein & Talcott, 1999). They are best thought of as individual differences between people rather than a consequence of neurological "disease".
