This 1997 theoretical paper by Stain and Walsh proposes a magnocellular hypothesis that accounts for evidence of irregularity of dyslexia across different modalities. The magnocellular theory considers magnocellular impairments as the primary cause for visual, auditory, and motor deficits that lead to phonological difficulties of dyslexic readers. The authors, referring to the early research (Lovegrove, Cornelisssn et al. and Galaburda et al.), argue that the deficient magnocellular pathway in the Lateral Geniculate Nucleus (LGN) could result in many perceptual temporal transit deficits. They acknowledge the mild amorality in LGN but also claim that the connection from the magnocellular laminate of the LGN to the posterior parietal cortex (PPC) may lead to many problems related to reading due to the importance of PPC in eye-movement control, visuospatial attention, and peripheral vision.…show more content… Moreover, the impaired PPC could contribute to the attention problem that would disrupt letter and word recognition and lead to the reduced peripheral vision. These problems would significantly impede reading of intensive texts. In addition to the visual modality, the authors also claim that the auditory subsystem responsible for analysing acoustic transients (similar to the magnocellular pathway) could cause low-level auditory transient processing. They even argue that the temporal processing deficits are even found in other domains such as motor systems. Therefore, Stain and Walsh propose a more broad consideration of the magnocellular hypothesis in which the deficits of dyslexia should be viewed from the aspects of visual, auditory and even motor temporal
