Abstract

Antisaccade performance in obsessive-compulsive disorder (OCD) is related to a dysfunctional network of brain structures including the (pre)frontal and posterior parietal cortices, basal ganglia, and superior colliculus. Previously recorded antisaccade performance of healthy and OCD subjects is re-analyzed to show greater variability in mean latency and variance of corrected antisaccades as well as in shape of antisaccade and corrected antisaccade latency distributions and increased error rates of OCD patients relative to healthy participants. Then a well-established neural accumulator model of antisaccade performance is employed to uncover the mechanisms giving rise to these observed OCD deficits. The model shows: i) increased variability in latency distributions of OCD patients is due to a more noisy accumulation of information by both correct and erroneous decision signals; (ii) OCD patients are almost as confident about their decisions as healthy controls; iii) competition via local lateral inhibition between the correct and erroneous decision processes, and not a third top-down STOP signal of the erroneous response, accounts for both the antisaccade performance of healthy controls and OCD patients.