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Clinical Implication of Altered Inhibitory Response in Patients with Post-traumatic Stress Disorder: Electrophysiological Evidence from a Go/Nogo Task

Title
Clinical Implication of Altered Inhibitory Response in Patients with Post-traumatic Stress Disorder: Electrophysiological Evidence from a Go/Nogo Task
Author
김성권
Keywords
PTSD; Go/Nogo; N2 latency; Cortical volume
Issue Date
2020-03
Publisher
SPRINGER
Citation
BRAIN TOPOGRAPHY, v. 33, no. 2, page. 208-220
Abstract
Inhibitory dysfunction is closely associated to post-traumatic stress disorder (PTSD). The present study investigated the neurophysiological evidence for and the brain regions related to inhibitory dysfunction in PTSD. Fifty patients with PTSD and 63 healthy controls (HCs) participated in a Go/Nogo task combined with electroencephalographic recordings. The N2–P3 complexes of event-related potentials (ERPs) elicited during the Nogo condition were compared between groups. Participants underwent structural magnetic resonance imaging to examine cortical volumes and completed questionnaires. Correlations between altered ERPs and cortical volumes of regions of interest as well as psychological symptoms were analysed. Nogo-N2 latencies at fve electrode sites (Fz, FCz, Cz, CPz, and Pz) were signifcantly delayed in patients with PTSD compared to HCs. Nogo-N2 latency had a signifcant negative correlation with the volume of gyrus in the inferior frontal cortex, orbitofrontal cortex, amygdala, and medial prefrontal cortex. Nogo-N2 latency was signifcantly and positively correlated with catastrophizing, anxiety, and perceived threat. These fndings show inhibitory dysfunction in patients with PTSD, refected by the delay in Nogo-N2 latencies. They also indicate that Nogo-N2 latencies are associated with smaller cortical volumes responsible for inhibition as well as with major symptoms of PTSD.
URI
https://www.proquest.com/docview/2376093699?accountid=11283https://repository.hanyang.ac.kr/handle/20.500.11754/163122
ISSN
1573-6792; 0896-0267
DOI
10.1007/s10548-020-00754-9
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ETC[S] > 연구정보
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