Modeling Cognitive Processing of Healthy Controls and Obsessive-Compulsive Disorder Subjects in the Antisaccade Task

Abstract

Antisaccade performance deficits in obsessive-compulsive disorder (OCD) include increased error rates and antisaccade latencies. These deficits are generally thought to be due to an impaired inhibitory process failing to suppress the erroneous response. The superior colliculus has been suggested as one of the loci of this impaired inhibitory process. Previously recorded antisaccade performance of healthy and OCD subjects is reanalyzed 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 compared to healthy controls. A neural accumulator model of the superior colliculus is then employed to uncover the biophysical mechanisms giving rise to the observed OCD deficits. The model shows that (i) the 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 less confident about their decisions than healthy controls, and (iii) competition via lateral inhibition between the correct and erroneous decision processes, and not a third independent inhibitory signal of the erroneous response, accounts for the antisaccade performance of healthy controls and OCD patients.