ABSTRACT
Disorganised cell layers in a part of the thalamus known as the lateral geniculate nucleus (LGN) have been found in dyslexia. This area of the thalamus is the relay point for visual stimuli from the retina of the eye to the visual cortex within the occipital lobe of the cerebrum. The thalamic cells that are disrupted are those of the magnocellular layers (Figure 15.1), large cells that convey sensory impulses relating to visual depth of fi eld and the visual perception of movement to the visual cortex. Other thalamic cells within the LGN, the parvocellular layers, which
convey colour and fi ne detail impulses to the cortex, are unaffected by the disorder. Pathways from the magnocellular layers of the LGN activate the part of the visual cortex called V5, which functions in the event of movement within the visual fi eld. In dyslexia, V5 activation by the sensory input from the LGN magnocellular layers appears not to happen. Reading is affected, possibly because words appear to the reader to move around on the page and become jumbled, and this is a common complaint made by those with dyslexia. They transpose letters within a word and this causes them to misread words; for example, the written word dog may be read as god. Perhaps the magnocellular layers are distorting the visual image of words and may be adding unnecessary movement, possibly in relation to the movement of the eyes themselves. Movement involves space, and other symptoms associated with dyslexia show disturbance to movement and space-related skills including poor handwriting, diffi culties with balance (e.g. when riding a bicycle), delayed walking skills and slowness in learning how to tell the time. These skills require visual input and the diffi culties found in dyslexia suggest problems associated with the development of the posterior parietal lobe, i.e. the primary visual cortex, or its input from the visual pathways via the LGN (Carlson 2010).
