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An inhibitory control is exerted when the context in which a movement has been planned changes abruptly making the impending movement inappropriate. Neurons in the frontal eye field and superior colliculus steadily increase activity before a saccadic eye movement, but cease the rise below a threshold when an impending saccade is withheld in response to an unexpected stop‐signal. This type of neural modulation has been majorly considered as an outcome of a race between preparatory and inhibitory processes ramping up to reach a decision criterion. An alternative model claims that the rate of saccade planning is diminished exclusively when the stop‐signal is detected within a stipulated period. However, due to a dearth of empirical evidence in support of the latter model, it remains unclear how the detectability of the stop‐signal influences saccade inhibition. In our study, human participants selected a visual target to look at by discriminating a go‐cue. Infrequently they cancelled saccade and reported whether they saw the stop‐signal. The go‐cue and stop‐signal both were embedded in a stream of irrelevant stimuli presented in rapid succession. Participants exhibited difficulty in detection of the stop‐signal when presented almost immediately after the go‐cue. We found a robust relationship between the detectability of the stop‐signal and the odds of saccade inhibition. Saccade latency increased exponentially with the maximum time available for processing the stop‐signal before gaze shifted. A model in which the stop‐signal onset spontaneously decelerated progressive saccade planning with the magnitude proportional to its detectability accounted for the data.

Tourette disorder (TD) is characterized by tics, which are sudden repetitive involuntary movements or vocalizations. Deficits in inhibitory control in TD patients remain inconclusive from the traditional method of estimating the ability to stop an impending action, which requires careful interpretation of a metric derived from race model. One possible explanation for these inconsistencies is that race model’s assumptions of independent and stochastic rise of GO and STOP process to a fixed threshold are often violated, making the classical metric to assess inhibitory control less robust. Here, we used a pair of metrics derived from a recent alternative model to address why stopping performance in TD is unaffected despite atypical neural circuitry. These new metrics distinguish between proactive and reactive inhibitory control and estimate them separately. When these metrics in adult TD group were contrasted with healthy controls (HC), we identified robust deficits in reactive control, but not in proactive control in TD. The TD group exhibited difficulty in slowing down the speed of movement preparation, which they rectified by their intact ability to postpone the movement.

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