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Contrast sensitivity was determined for dyslexic and normal readers. When testing with temporally ramped (i.e. stimuli with gradual temporal onsets and offsets) gratings of 0.6, 4.0, and 12.0 cycles/deg, we found no difference in contrast sensitivity between dyslexic readers and controls. Using 12.0 cycles/deg gratings with transient (i.e. abrupt) onsets and offsets, we found that dyslexic individuals had, compared to controls, markedly inferior contrast sensitivity at the shortest stimulus durations (i.e. 17, 34, and 102 ms). This deficit may reflect more sluggish temporal summation. There was no difference in sensitivity to 0.6 cycles/deg gratings with transient onsets and offsets. Under these conditions, the two groups showed a consistent and equal increase in sensitivity relative to the ramped baseline condition at 0.6 cycles/deg at the longer stimulus durations. This demonstrates that dyslexic readers have no deficit in their ability to detect stimulus transients, a finding which appears to be inconsistent with a transient system deficit. That detection of the low-frequency stimuli was mediated by the transient system is further indicated by the fact that these stimuli were more susceptible to forward masking than were the high-frequency stimuli. The effects of masking of both high and low spatial-frequency stimuli were about equal for dyslexic readers and controls. This is not in agreement with the transient system deficit theory, according to which one would expect there to be less masking of high spatial-frequency stimuli in the case of dyslexic readers.

Numerous studies have found that visual deficits are associated with dyslexia. The prevailing theory regarding this association is that dyslexia is the result of a deficit in the magnocellular system (earlier called the transient system) in the visual pathway. An essential assumption of this theory is that the parvocellular system (formerly called the sustained system) is suppressed by the magnocellular system at the time of saccadic eye movements. This assumption is examined on the basis of published studies of saccadic suppression. The evidence from six studies indicates quite unequivocally that the magnocellular system, not the parvocellular system, is suppressed during saccadic eye movements. It seems, therefore, that an essential premise of the magnocellular deficit theory of dyslexia is incorrect.