Increased anterior brain activation to correct responses on high-conflict Stroop task in obsessive–compulsive disorder

Abstract Objective An abnormally increased activation in anterior brain networks, accompanied by normal task performance, has been reported in studies on biological mechanisms of obsessive–compulsive disorder (OCD). We test a hypothesis, that this phenomenon, deemed specific to OCD, will be compromi...

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Veröffentlicht in:Clinical neurophysiology 2011-01, Vol.122 (1), p.107-113
Hauptverfasser: Ciesielski, Kristina T, Rowland, Laura M, Harris, Richard J, Kerwin, Audra A, Reeve, Alya, Knight, Jeanne E
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Sprache:eng
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Zusammenfassung:Abstract Objective An abnormally increased activation in anterior brain networks, accompanied by normal task performance, has been reported in studies on biological mechanisms of obsessive–compulsive disorder (OCD). We test a hypothesis, that this phenomenon, deemed specific to OCD, will be compromised by a very difficult task, which may lead to reduced cortical information processing and erroneous performance, as found in other disorders such as schizophrenia. Methods We designed a new variant of high-conflict Stroop-word-color interference task (Stroop-WCIT) with each incongruent (INC) trial preceded by multiple congruent trials. Event-related potentials (ERPs) were acquired from subjects with OCD and case-matched healthy controls (C). We analyzed ERPs elicited by correct responses to conflict-related INC trials. Results Our hypothesis found no support. Although the anterior ERPs N200, a negative component within 140–300 ms latency window, was significantly abnormally increased in OCD subjects, their performance accuracy remained normal. Conclusions Current findings suggest an enhanced adaptive top-down control in OCD mediated by the prefrontal lateral and dorsal anterior cingulate networks. Significance Further studies are warranted to test the hypothesis that increased activity within the anterior network for top-down inhibitory control in OCD may be a part of an adaptive compensatory neural mechanism.
ISSN:1388-2457
1872-8952
DOI:10.1016/j.clinph.2010.05.027