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Background: We used ocular motor paradigms to examine whether or not saccades are impaired in individuals with high functioning autism (HFA). Methods: We recorded eye movements in patients with HFA (n=11), and in normal adolescents (n=11) on anti-saccade, memory-guided saccade (MGS), predictive saccade and gap/overlap tasks. Results: Compared with the normal subjects, patients with HFA had (1) a significantly higher percentage of directional errors on the anti-saccade task (63.2% versus 26.6%), (2) a significantly higher percentage of response suppression errors on a MGS task (60.3% versus 29.5%) and (3) a significantly lower percentage of predictive eye movements on a predictive saccade task. They also showed longer latencies on a MGS task and for all conditions tested on a gap/null/overlap task (fixation target extinguished before, simultaneously, or after the new peripheral target appeared). When the latencies during the gap condition were subtracted from the latencies in the overlap condition, there was no difference between patients and normals. Conclusions: Abnormalities in ocular motor function in patients with HFA provide preliminary evidence for involvement of a number of brain regions in HFA including the dorsolateral prefrontal cortex (dlPFC) and the frontal eye fields (FEFs) and possibly the basal ganglia and parietal lobes.

Studies of eye movements in patients with Huntington's disease (HD) have suggested that frontal lobe-basal ganglia structures are more involved in HD than the parietal lobes. To test this hypothesis further we compared the ability of HD patients and normal subjects to direct “covert” visual attention, using saccade latency and thumb press reaction time tasks that have been shown to be sensitive to parietal lobe dysfunction. Subjects were instructed to move their eyes or to press a button when a peripheral target was illuminated. The peripheral stimulus appeared at various intervals after the appearance of a central arrow(s) that pointed in the direction of the target (valid cue), in the opposite direction (invalid cue), or pointed simultaneously in both directions (neutral cue). For both saccade and thumb press paradigms, the difference in the latencies for trials with invalid and valid cues was the same in HD patients and normals. These findings suggest that the ability to direct visual attention is normal in HD and are compatible with the hypothesis that in HD, frontal-basal ganglia circuits are more affected than parietal lobe pathways.