Countermanding saccades in humans

AbstractWe used a countermanding paradigm to investigate the relationship between conflicting cues for controlling human saccades. Subjects made a saccade to a target appearing suddenly in the periphery; but on some trials, after a delay, a stop-signal was presented that instructed subjects to inhibit the saccade. As we increased this delay, subjects increasingly failed to inhibit the movement. From measurements of this relationship, and of saccadic latency in control trials, we estimated the average time needed to inhibit the saccade (the stop-signal reaction time or SSRT). SSRTs were similar across subjects, between 125 and 145 ms, and did not vary with target luminance. We then investigated a race model in which the target initiates a response preparation signal rising linearly with a rate varying randomly from trial to trial, and racing against a similarly rising signal initiated by the cue to inhibit the saccade. The first process to cross a trigger threshold determines whether the saccade is initiated or not. In Monte Carlo simulations, this model correctly predicted the probability of successful saccade inhibition as a function of the stop-signal delay, and also the statistical distributions of saccadic latency during trials in which a stop-signal was presented but the subject failed to inhibit the saccade. These findings provide a comparison to results previously described in the monkey, and show that a simple race model with a linear rise to threshold may underlie behavioural performance in tasks of this kind

Influence of history on countermanding performance in humans and macaque monkeys

The stop-signal or countermanding task probes the ability to control action by requiring subjects to withhold a planned movement in response to an infrequent stop signal which they do with variable success depending on the delay of the stop signal. We investigated whether performance of humans and macaque monkeys in a saccade countermanding task was influenced by stimulus and performance history. In spite of idiosyncrasies across subjects several trends were evident in both humans and monkeys. Response time decreased after successive trials with no stop signal. Response time increased after successive trials with a stop signal. However, post error slowing was not observed. Increased response time was observed mainly or only after cancelled (signal inhibit) trials and not after noncancelled (signal respond) trials. These global trends were based on rapid adjustments of response time in response to momentary fluctuations in the fraction of stop signal trials. The effects of trial sequence on the probability of responding were weaker and more idiosyncratic across subjects when stop signal fraction was fixed. However, both response time and probability of responding were influenced strongly by variations in the fraction of stop signal trials. These results indicate that the race model of countermanding performance requires extension to account for these sequential dependencies and provide a basis for physiological studies of executive control of countermanding saccade performance