a1 Department of Psychiatry, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Cambridge, UK
a2 Behavioural and Clinical Neuroscience Institute (BCNI), University of Cambridge, Cambridge, UK
a3 Department of Psychiatry, Queen Elizabeth II Hospital, Welwyn Garden City, Hertfordshire, UK
a4 Postgraduate Medical School, University of Hertfordshire, Hatfield, UK
a5 Department of Experimental Psychology, University of Cambridge, Cambridge, UK
Background Obsessive-compulsive disorder (OCD) has been associated with impairments in stop-signal inhibition, a measure of motor response suppression. The study used a novel paradigm to examine both thought suppression and response inhibition in OCD, where the modulatory effects of stimuli relevant to OCD could also be assessed. Additionally, the study compared inhibitory impairments in OCD patients with and without co-morbid depression, as depression is the major co-morbidity of OCD.
Method Volitional response suppression and unintentional thought suppression to emotive and neutral stimuli were examined using a novel thought stop-signal task. The thought stop-signal task was administered to non-depressed OCD patients, depressed OCD patients and healthy controls (n=20 per group).
Results Motor inhibition impairments were evident in OCD patients, while motor response performance did not differ between patients and controls. Switching to a new response but not motor inhibition was affected by stimulus relevance in OCD patients. Additionally, unintentional thought suppression as measured by repetition priming was intact. OCD patients with and without depression did not differ on any task performance measures, though there were significant differences in all self-reported measures.
Conclusions Results support motor inhibition deficits in OCD that remain stable regardless of stimulus meaning or co-morbid depression. Only switching to a new response was influenced by stimulus meaning. When response inhibition was successful in OCD patients, so was the unintentional suppression of the accompanying thought.
(Received November 05 2008)
(Revised April 23 2009)
(Accepted May 13 2009)
(Online publication July 02 2009)
c1 Address for correspondence: S. Morein-Zamir, Ph.D., Box 189, Level 4, Department of Psychiatry, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK. (Email: firstname.lastname@example.org)