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Inicio Porto Biomedical Journal Voluntary inhibition of saccadic eye movements: EEG study
Información de la revista
Vol. 2. Núm. 5.
Páginas 207-208 (septiembre - octubre 2017)
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Vol. 2. Núm. 5.
Páginas 207-208 (septiembre - octubre 2017)
PS190
Open Access
Voluntary inhibition of saccadic eye movements: EEG study
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1458
A. Fedotova
Autor para correspondencia
fedotova.brain@gmail.com

Corresponding author.
, M. Slavutskaya
Lomonosov Moscow State University, Department of Higher Nervous Activity, Russia
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Aim: The aim of our study was to find out EEG markers of inhibitory control in human.

Introduction: The voluntary inhibition is an important component of cognitive control. It is strong in healthy adults and weak in people with schizophrenia. The cortical mechanisms of inhibition are associated with event-related potentials (ERPs). In the case of a saccadic response some new EEG correlates of inhibition could be found.

Methods: Sixteen healthy right-handed subjects (18–22 years) participated in the study. We used a modified “Go/No go delay” paradigm with long interstimulus interval (2800–3000ms). The task involved two types of target stimuli (“Go”, “No go”) with 50% probability. EEG and saccades were recorded simultaneously. ERPs were determined by means of coherent averaging relative to target stimulus onset. The EEG brain mapping was used to depict spatial dynamics of P1.

Results: P1 peak latency was 90–140ms and tended to increase in cases of inhibition (by 6±0.5ms, p<0.05). In the “No go” situation P1 amplitude was significantly lower than that in case of “Go” stimulus presentation (by 3.3±0.7mkV, p<0,05). Regardless of the place where “No go” stimulus appeared, P1 amplitude was significantly higher on the right hemisphere, that is known to be the dominant one for inhibitory control. The EEG mapping data demonstrate the “bottom-up” spreading of P1 foci in “No go” conditions. It also indicates inhibitory processes.

Conclusion: The spatiotemporal parameters of P1 component in “Go/No go delay” paradigm reflect inhibitory processes. Therefore, P1 can be used as EEG marker of inhibitory violations in the clinical research. Our current research involves as subjects the patients with schizophrenia and ultra-high risk patients, as they demonstrate weakened the inhibitory processes. The data would contribute to the reliable diagnostics of schizophrenia at its early stages and to the plausible correction of cognitive impairments.

Acknowledgements: I would like to express my sincere gratitude to my supervisor D.Sc. in Biology Maria V. Slavutskaya.

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