Sequence effects and SSD are associated with N2 and P3 signals during stopping in a visual stop signal task
- 1Department of Psychology, University of Oslo, Oslo, Norway
- 2Department of Computer Science and Communication, Østfold University College, Halden, Norway
Abstract
Studies combining the stop signal task (SST) with Electroencephalogram (EEG) have often asked whether the frontocentral N2 and P3 components are influenced by failed versus successful stopping. Estimates of the N2 and P3 commonly reflect averages across experimental trials per individual allowing for assessing mean-level effects. The probability of responding to a stop trial is influenced by task parameters such as the stop signal delay and the asymmetric presentation frequency of Go and Stop trials. Trial-by-trial variation in task parameters like the stop signal delay have been shown to influence brain activity differences between stop outcomes in fMRI data but have not been investigated in EEG data. Changes in the global frequency of Go and Stop trials have been shown to influence behavioral performance and the N2 and P3 components but potential influences of local sequential dependencies that may arise on a trial-by-trial basis have simply been ignored. It is possible that both the SSD and local sequential dependencies arising from past trial histories systematically influence N2 and P3 amplitudes or latencies during stopping. This study used mixed effects modeling to assess associations between SSD, sequential dependencies, and single trial estimates of latency and amplitude of the N2 and P3 components during failed and successful stopping. We specified interactions between both predictor variables and the two stop outcomes. The results showed complex curvilinear associations between the latency of the N2 and P3 components with SSD. Longer SSDs were associated with shorter latencies while only the N2 showed significant interaction with stop outcomes. Sequential dependencies were significantly associated with the N2 and P3 amplitudes. A longer series of go trials was associated with more negative N2 amplitudes and more positive P3 amplitudes. The N2 amplitude was larger after having recently encountered a stop trial, while the P3 amplitude increased at a similar rate during both failed and successful stopping. Together, these results indicate that accounting for the influence of SSD and sequential dependencies on ERP estimates of the N2 and P3 components is of high importance, particularly in studies comparing clinical to healthy control participants.
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BibTeX
@article{skaug2026sequence,
title = {{Sequence effects and SSD are associated with N2 and P3 signals during stopping in a visual stop signal task}},
author = {Knut Andre Skaug and Lars Vidar Magnusson and Rene Jürgen Huster},
journal = {Frontiers in Human Neuroscience},
year = {2026},
month = oct,
doi = {10.3389/fnhum.2026.1906495},
url = {https://doi.org/10.3389/fnhum.2026.1906495},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Sequence effects and SSD are associated with N2 and P3 signals during stopping in a visual stop signal task
AU - Knut Andre Skaug
AU - Lars Vidar Magnusson
AU - Rene Jürgen Huster
PY - 2026
DA - 2026/10/12
JO - Frontiers in Human Neuroscience
DO - 10.3389/fnhum.2026.1906495
UR - https://doi.org/10.3389/fnhum.2026.1906495
AB - Studies combining the stop signal task (SST) with Electroencephalogram (EEG) have often asked whether the frontocentral N2 and P3 components are influenced by failed versus successful stopping. Estimates of the N2 and P3 commonly reflect averages across experimental trials per individual allowing for assessing mean-level effects. The probability of responding to a stop trial is influenced by task parameters such as the stop signal delay and the asymmetric presentation frequency of Go and Stop trials. Trial-by-trial variation in task parameters like the stop signal delay have been shown to influence brain activity differences between stop outcomes in fMRI data but have not been investigated in EEG data. Changes in the global frequency of Go and Stop trials have been shown to influence behavioral performance and the N2 and P3 components but potential influences of local sequential dependencies that may arise on a trial-by-trial basis have simply been ignored. It is possible that both the SSD and local sequential dependencies arising from past trial histories systematically influence N2 and P3 amplitudes or latencies during stopping. This study used mixed effects modeling to assess associations between SSD, sequential dependencies, and single trial estimates of latency and amplitude of the N2 and P3 components during failed and successful stopping. We specified interactions between both predictor variables and the two stop outcomes. The results showed complex curvilinear associations between the latency of the N2 and P3 components with SSD. Longer SSDs were associated with shorter latencies while only the N2 showed significant interaction with stop outcomes. Sequential dependencies were significantly associated with the N2 and P3 amplitudes. A longer series of go trials was associated with more negative N2 amplitudes and more positive P3 amplitudes. The N2 amplitude was larger after having recently encountered a stop trial, while the P3 amplitude increased at a similar rate during both failed and successful stopping. Together, these results indicate that accounting for the influence of SSD and sequential dependencies on ERP estimates of the N2 and P3 components is of high importance, particularly in studies comparing clinical to healthy control participants.
SN - 1662-5161
ER -