The severe deficits in rapid automatized naming demonstrated by children with developmental dyslexia has usually been interpreted in terms of a deficit in speed of access to the lexicon rather than as a possible deficit in speed of visual object recognition. Yet fluent reading requires rapid visual recognition and semantic interpretation of new letters and words appearing in successive fixations of the eyes. Thus we wondered whether change detection performance was related to reading ability. We investigated whether children with developmental dyslexia (DD) were less able to detect change in a simple display--gap--display paradigm than normal reading (NR) children of the same age and children with impaired reading and mentation (LD). In a first experimental phase, the DDs required a longer initial exposure of four letter items in order to detect change of a single letter at a level of 71% correct, compared with NRs performing at the same level. Thus the deficit in reading in DD is associated with a deficit in early processes associated with visual recognition. In a second experimental phase (using the individual target display exposures measured in the first phase), cues appeared during the 250 ms gap for a period of either 0 (no cue), 50 or 200 ms immediately prior to the presentation of the second (comparison) display. Children of all groups showed dependence on the presence of the cue to help make a judgement of change (versus no change), with the NRs least affected. When change was detected in the presence of a cue, the NRs were better able to identify the new letter than either of the other groups. However, only about 50% of the correct detections were accompanied by a correct identification. Despite published reports of a mini-neglect for left visual field in dyslexic adults, none of our groups showed such an effect. However, a significant upper visual field (UpVF) advantage in change detection performance was found across groups, which we interpret in terms of the interactions of the ventral and dorsal streams.

The ability to detect change has not been well studied in children.A research paradigm was used involving search for a change made to one of four letter targets, presented twice, with a gap of 250 ms.Sixty-one schoolchildren, aged 7.3 - 12.9 years,participated in the study. The duration of the first presentation was such that each child was detecting change at a rate of 71% correct. The mean duration was 0.91 s (SD = 0.58 s),with older children not significantly faster in detecting change. In the second phase, using the duration established in the first phase, the effect of cue condition on detection was studied. An upper visual field advantage for change detection was clearly evident for un-cued trials. The most likely explanation derives from the masking produced by the reappearance of the four targets, which interferes with the process of change detection. The greater dorsal pathway representation of the lower visual field implies greater masking there, yielding better change detection in the upper visual field.

Developmental dyslexia, a specific learning difficulty in reading, manifests as effortful decoding of words and as such is commonly associated with reduced phonemic awareness. However, its underlying cause remains elusive, with magnocellular visual processing, temporal auditory processing, visual attentional deficits and cerebellar dysfunction all gaining some traction. More recent theories have concerned visual attention span, measuring the parallel attentive capacity of the sensory visual system.

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The neural basis of dyslexia remains unresolved, despite many theories relating dyslexia to dysfunction in visual magnocellular and auditory temporal processing, cerebellar dysfunction, attentional deficits, as well as excessive neural noise. Recent research identifies perceptual speed as a common factor, integrating several of these systems. Optimal perceptual speed invokes transient attention as a necessary component, and change detection in gap paradigm tasks is impaired in those with dyslexia. This research has also identified an overall better change detection for targets presented in the upper compared with lower visual fields. Despite the magnocellular visual pathway being implicated in the aetiology of dyslexia over 30 years ago, objective physiological measures have been lacking. Thus, we employed nonlinear visual evoked potential (VEP) techniques which generate second order kernel terms specific for magno and parvocellular processing as a means to assessing the physiological status of poor readers (PR, n=12) compared with good readers (GR, n=16) selected from children with a mean age of 10yr. The first and second order Wiener kernels using multifocal VEP were recorded from a 4° foveal stimulus patch as well as for upper and lower visual field peripheral arcs. Foveal responses showed little difference between GR and PR for low contrast stimulation, except for the second slice of the second order kernel where lower peak amplitudes were recorded for PR vs GR. At high contrast, there was a trend to smaller first order kernel amplitudes for short latency peaks of the PR vs GR. In addition, there were significant latency differences for the first negativity in the first two slices of the second order kernel. In terms of peripheral stimulation, lower visual field response amplitudes were larger compared with upper visual field responses, for both PR and GR. A trend to larger second/first order ratio for magnocellularly driven responses suggests the possibility of lesser neural efficiency in the periphery for the PR compared with the GR. Stronger lower field peripheral response may relate to better upper visual field change detection performance when target visibility is controlled through flicking masks. In conclusion, early cortical magnocellular processing at low contrast was normal in those with dyslexia, while cortical activity related to parvocellular afferents was reduced. In addition, the study demonstrated a physiological basis for upper versus lower visual field differences related to magnocellular function.