In five experiments we compared prosaccade and antisaccade performance in normal human observers. This was first examined for visual stimulation in temporal or nasal hemifields, under monocular viewing. Prosaccades were faster following temporal than nasal stimulation, in accordance with previous results. The novel finding was that the opposite pattern was observed for antisaccades, consistent with a difficulty in overcoming a stronger prosaccade tendency after temporal-hemifield stimulation. A second experiment showed that these results were not simply due to antisaccades following nasal stimulation benefitting from being made towards a temporal place-holder. Prosaccades and antisaccades were then compared for visual versus somatosensory stimulation. The substantial latency difference between prosaccades and antisaccades for visual stimuli was eliminated for somatosensory stimuli. Antisaccades can thus benefit in relative terms when the competing prosaccadic tendency is weakened; but two further experiments revealed that not all manipulations induce opposing outcomes for the two types of saccade. Although reducing the contrast of visual targets can slow prosaccades and conversely speed antisaccades, this was not the case at the lowest contrast level used, where both types of saccade were slowed, thus indicating some common limiting source. Moreover, warning sounds presented shortly before a visual target speeded both prosaccades and antisaccades. These results illustrate that several factors which slow prosaccades can speed antisaccades (consistent with competition between different pathways); but also reveal some notable exceptions, where both types of saccade are slowed or speeded together, suggesting some common pathways that may precede competition over the direction of the saccade.

An important characteristic of autism spectrum disorder (ASD) is increased visual detail perception. Yet, there is no standing neurobiological explanation for this aspect of the disorder. We show evidence from EEG data, from 31 control subjects (three females) and 13 subjects (two females) aged 16-28 years, for a specific impairment in object boundary detection in ASD, which is present as early as 120 ms after stimulus presentation. In line with a neural network model explicating the role of feedforward, horizontal and recurrent processing in visual perception, we can attribute this deficit to a dysfunction of horizontal connections within early visual areas. Interestingly, ASD subjects showed an increase in subsequent activity at lateral occipital sites (225 ms), which might reflect a compensational mechanism. In contrast, recurrent processing between higher and lower visual areas (around 260 ms), associated with the segregation between figure and background, was normal. Our results show specific neural abnormalities in ASD related to low-level visual processing. In addition, given the reconciliation between our findings and previous neuropathology and neurochemistry research, we suggest that atypical horizontal interactions might reflect a more general neural abnormality in this disorder.