Although current research is exploring numerous possible causes, the magnocellular theory, in particular, has recently gained much attention. This theory suggests that a deficit in the magnocellular pathway (MC) may be responsible for the visual, learning, and processing problems found in dyslexia. Because the MC pathway, along with the parvocellular pathway, connects the retina to the occipital and parietal lobes of the brain, it allows information brought in by the eye to be processed by the necessary areas of the brain. The MC pathway, therefore, is believed to be a crucial component of several different visual processes.Included in these processes is its ability to receive stimuli at low frequencies and low luminance levels, thus allowing us to perceive low wavelengths of light and gather information even in relative darkness. This pathway is also particularly sensitive to visual motion, and direction of movement and gaze. It is this system, therefore, that detects the direction and meaning of objects in motion, while remaining "blind" to details such as color. In addition, the magnocellular pathway helps control eye movement.
Recent studies have suggested that many of the functional deficits found in dyslexics are processes controlled by the magnocellular pathway. Researchers have found that most dyslexics show a reduced contrast sensitivity at low spatial frequencies and low luminance levels. This implies that their visual abilities are impaired in times of low light. Visual motion sensitivity, regardless of the frequency and illumination levels, is also greatly impaired. Recent evidence gathered by both elicited potential and MRI studies have supported this visual motion deficit. All of these deficits indicate a possible disruption to the magnocellular pathway. (Stein, et al., 1997).
In addition, it is believed that faulty control of binocular eye movements may be responsible for the moving and blurred images reported by many dyslexics. If the magnocellular pathway does indeed control eye movement, then a disruption to this system could account for the dyslexic's distorted images.
By far, however, the strongest physical data implicating the MC pathway lies in the postmortem study of five dyslexic brains. These studies showed the magnocells to be disordered and over 20% smaller than cells in normal brains. (Galaburda, 1985)
Although this evidence points to a defect in the magnocellular pathway, researchers are still left trying to understand what role these defects play in reading and learning disorders. The answers, they believe, lie in the parietal and temporal regions of the cortex, both of which process magnocellular information. In particular, the posterial parietal cortex is involved in visual-spatial attention, peripheral vision, eye movement control, and attention tasks. Being able to have the proper control over eye movement and the attention to concentrate and remain focused are crucial to reading and learning skills. Because these lobes are the final destination of the magnocellular pathway, researchers believe that it is these small defects in the MC pathway that can lead to greatly amplified deficits of the parietal cortex.In the temporal lobe, recent MRI evidence has identified a deficit in the V5 region of dyslexic brains. When dyslexics are asked to read or follow moving dots, this region, responsible for processing rapid visual motion, lacks normal activity (Travis, 1996). It seems, therefore, that the strongest evidence to date points to dysfunction of the tempo-parietal regions of the brain.
No comments:
Post a Comment