Format

Send to

Choose Destination
Psychol Med. 2013 Feb;43(2):391-400. doi: 10.1017/S0033291712001018. Epub 2012 May 14.

Punishment promotes response control deficits in obsessive-compulsive disorder: evidence from a motivational go/no-go task.

Author information

1
MRC/Wellcome Trust Behavioural and Clinical Neuroscience Institute (BCNI), Department of Experimental Psychology, University of Cambridge, Cambridge, UK. sm658@cam.ac.uk

Abstract

BACKGROUND:

Obsessive-compulsive disorder (OCD) has been associated with response inhibition deficits under motivationally neutral contingencies. We examined response inhibition performance in the presence of reward and punishment. We further investigated whether the hypothesized difficulties in flexibly updating behaviour based on external feedback in OCD would also lead to a reduced ability to adjust to changes in the reward and punishment contingencies.

METHOD:

Participants completed a go/no-go task that used punishments or rewards to promote response activation or suppression. The task was administered to OCD patients free of current Axis-I co-morbidities including major depression (n = 20) and a group of healthy controls (n = 32).

RESULTS:

Compared with controls, patients with OCD had increased commission errors in punishment conditions, and failed to slow down immediately after receiving punishment. The punishment-induced increase in commission errors correlated with self-report measures of OCD symptom severity. Additionally, patients did not differ from controls in adapting their overall response style to the changes in task contingencies.

CONCLUSIONS:

Individuals with OCD showed reduced response control selectively under punishment conditions, manifesting in an impulsive response style that was related to their current symptom severity. This stresses failures of cognitive control in OCD, particularly under negative motivational contingencies.

PMID:
22578546
PMCID:
PMC3544546
DOI:
10.1017/S0033291712001018
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Cambridge University Press Icon for PubMed Central
Loading ...
Support Center