Stop-signal response inhibition in schizophrenia: Behavioural, event-related potential and functional neuroimaging data

2012 ◽  
Vol 89 (1) ◽  
pp. 220-231 ◽  
Author(s):  
Matthew Edward Hughes ◽  
William Ross Fulham ◽  
Patrick James Johnston ◽  
Patricia Therese Michie
2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S63-S63
Author(s):  
Ya Wang ◽  
Lu-xia Jia ◽  
Xiao-jing Qin ◽  
Jun-yan Ye ◽  
Raymond Chan

Abstract Background Schizotypy, a subclinical group at risk for schizophrenia, have been found to show impairments in response inhibition. Recent studies differentiated proactive inhibition (a preparatory process before the stimuli appears) and reactive inhibition (the inhibition of a pre-potent or already initiated response). However, it remains unclear whether both proactive and reactive inhibition are impaired in schizotypy and what are the neural mechanisms. The present event-related potential study used an adapted stop-signal task to examine the two inhibition processes and the underlying neural mechanisms in schizotypy compared to healthy controls (HC). Methods A total of 21 individuals with schizotypy and 25 matched HC participated in this study. To explore different degrees of proactive inhibition, we set three conditions: a “certain” go condition which no stop signal occurred, a “17% no go” condition in which stop signal would appear in 17% of trials, and a “33% no go” condition in which stop signal would appear in 33% of trials. All participants completed all the conditions, and EEG was recorded when participants completed the task. Results Behavioral results showed that in both schizotypy and HC, the reaction times (RT) of go trials were significantly prolonged as the no go percentage increased, and HC showed significantly longer go RT compared with schizotypy in both “17% no go” and “33% no go” conditions, suggesting greater proactive inhibition in HC. Stop signal reaction times (SSRTs) in “33% no go” condition was shorter than “17% no go” condition in both groups. Schizotypy showed significantly longer SSRTs in both “17% no go” and “33% no go” conditions than HC, indicating schizotypy relied more on reactive inhibition. ERP results showed that schizotypy showed larger overall N1 for go trials than HC irrespective of condition, which may indicate a compensation process in schizotypy. Schizotypy showed smaller N2 on both successful and unsuccessful stop trials in “17% no go” conditions than HC, while no group difference was found in “33% no go” conditions for stop trials, which may indicate impaired error processing. Discussion These results suggested that schizotypy tended to be impaired in both proactive control and reactive control processes.


2012 ◽  
Vol 85 (1) ◽  
pp. 93-105 ◽  
Author(s):  
Magdalena Senderecka ◽  
Anna Grabowska ◽  
Jakub Szewczyk ◽  
Krzysztof Gerc ◽  
Roman Chmylak

NeuroImage ◽  
2009 ◽  
Vol 47 ◽  
pp. S180
Author(s):  
NC Swann ◽  
N Tandon ◽  
RT Canolty ◽  
TM Ellmore ◽  
LK McEvoy ◽  
...  

2015 ◽  
Vol 22 (7) ◽  
pp. 639-650 ◽  
Author(s):  
Tieme W. P. Janssen ◽  
Dirk J. Heslenfeld ◽  
Rosa van Mourik ◽  
Katleen Geladé ◽  
Athanasios Maras ◽  
...  

Objective: Deficits in response inhibition figure prominently in models of ADHD; however, attentional deficiencies may better explain previous findings of impaired response inhibition in ADHD. We tested this hypothesis at the neurophysiological level. Method: Dense array ERPs (event-related potentials) were obtained for 46 children with ADHD and 51 controls using the stop-signal task (SST). Early and late components were compared between groups. N2 and P3 components were localized with LAURA distributed linear inverse solution. Results: A success-related N1 modulation was only apparent in the ADHD group. N2 and P3 amplitudes were reduced in ADHD. During the successful inhibition N2, the ADHD group showed reduced activation in right inferior frontal gyrus (rIFG), supplementary motor area (SMA), and right temporoparietal junction (rTPJ), and during failed inhibition in the rIFG. During the successful inhibition P3, reduced activation was found in anterior cingulate cortex (ACC) and SMA. Conclusion: Impairments in the ventral attention network contribute to the psychopathology of ADHD and challenge the dominant view that ADHD is underpinned by impaired inhibitory control.


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