Functional Neuroimaging of Avoidance Habits in Obsessive-Compulsive Disorder
Urcelay, Gonzalo P
Fineberg, Naomi A
- Publisher: The American Journal of Psychiatry
Objective: The goal of this study was to determine the neural correlates of excessive habit formation in obsessive-compulsive disorder (OCD). We aimed to (i) test for neurobiological convergence with the known pathophysiology of OCD and (ii) infer, based on abnormalities in brain activation, whether these habits arise from dysfunction in the goal-directed or habit system.
Method: Thirty-seven OCD patients and 33 controls learned to avoid shocks while undergoing a functional Magnetic Resonance Imaging (fMRI) scan. Following 4 blocks of training, we tested if the avoidance response had become a habit by removing the threat of shock and measuring continued avoidance. We tested for task-related differences in brain activity in 3 ROIs, the caudate, putamen and medial orbitofrontal cortex at a statistical threshold of p<.05, family-wise error (FWE) corrected.
Results: We observed excessive habit formation in OCD patients, which was associated with hyper-activation in the caudate. Activation in this region was also associated with subjective ratings of increased urge to perform habits. The OCD group, as a whole, showed hyper-activation in the medial orbitofrontal cortex (mOFC) during the acquisition of avoidance, however this did not relate directly to habit formation.
Conclusions: OCD patients exhibited excessive habits that were associated with hyper-activation in a key region implicated in the pathophysiology of OCD, the caudate nucleus. Prior studies suggest that this region is important for goal-directed behavior, suggesting that habit-forming biases in OCD may be a result of impairments in this system, rather than differences in the build up of stimulus-response habits themselves.
This research was funded by a Wellcome Trust grant (089589/Z/09/Z) awarded to TW Robbins, BJ Everitt, AC Roberts, JW Dalley and BJ Sahakian. Work was completed at the Behavioural and Clinical Neuroscience Institute, which is supported by a joint award from the Medical Research Council and Wellcome Trust (G00001354). Dr Gillan is supported by a Sir Henry Wellcome Postdoctoral Fellowship (101521/Z/12/Z). Dr Apergis-Schoute and Dr Morein-Zamir are supported by the Wellcome Trust grant above (089589/Z/09/Z).
Published by The American Journal of Psychiatry where the final published version can be found at http://dx.doi.org/10.1176/appi.ajp.2014.14040525
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