Elsevier

Psychiatry Research

Volume 120, Issue 3, 15 October 2003, Pages 265-271
Psychiatry Research

Reduced response-inhibition in obsessive–compulsive disorder measured with topographic evoked potential mapping

https://doi.org/10.1016/S0165-1781(03)00188-4Get rights and content

Abstract

Recent neuroimaging studies have suggested that a hyperactivity of the frontal-striate neuronal circuits, including the orbitofrontal cortex and the basal ganglia, mediates the symptomatology of obsessive–compulsive disorder (OCD). However, there is also some evidence that the superior frontal cortex is less activated in OCD, and this local hypoactivity has been shown to be negatively associated with the symptomatology. As the superior frontal cortex is believed to be involved in inhibitory control, this study investigated the brain electrical activity during response inhibition in OCD. Twelve patients with OCD and 12 healthy controls performed a cued Go–NoGo task (continuous performance test), while event-related potentials were registered with 21 electrodes. Patients reacted significantly faster than controls, but did not differ from controls regarding the error rate. As a main result, we found a reduced frontal activity during the NoGo condition in OCD, which was condensed in a reduced anteriorisation of the brain electrical field. We suggest that this inhibitory deficit in OCD has a major contribution to the pathophysiology of OCD, which is underscored by the fact that the anteriorisation during the NoGo condition (NGA) was negatively correlated with the symptomatology as measured by the Yale-Brown Obsessive-Compulsive Scale.

Introduction

Patients with obsessive–compulsive disorder (OCD) can be characterised as being impaired in the inhibition of repetitive thoughts and behaviour. This clinical observation was confirmed by neuropsychological studies showing a deficit in inhibitory processes (Martinot et al., 1990, Rosenberg et al., 1997a, Rosenberg et al., 1997b) amongst other impairments (Purcell et al., 1998, Schmidtke et al., 1998), all indicating a disturbance of frontal lobe functioning. Neuroimaging studies showed increased activity consistently in the orbitofrontal cortex and the caudate nucleus, under resting conditions (Baxter et al., 1987, Saxena et al., 1999, Swedo et al., 1989) as well as under symptom provocation (Adler et al., 2000, Breiter and Rauch, 1996, Rauch et al., 1994). This hyperactivity is correlated with the symptomatology (McGuire et al., 1994) and normalises after therapy (Benkelfat et al., 1990, Swedo et al., 1992). However, as this hyperactivity was found not only in patients with OCD, but also in specific phobias and post-traumatic stress disorder under symptom provocation, it has been argued that hyperactivity might reflect anxiety more than the specific neuronal correlates of OCD (Rauch et al., 1997). Furthermore, it was shown that the activity of the right superior frontal cortex was negatively correlated with the OCD symptomatology (Adler et al., 2000, McGuire et al., 1994). This association was interpreted as a sign for inhibitory processes, which seem to be most relevant to the understanding of OCD. In accordance with the above-mentioned inhibitory deficits in patients with OCD, reduced activity during resting conditions was found in the superior frontal cortex (Lucey et al., 1995).

In order to analyse the brain activity related to inhibitory processes in more detail, it might be useful to measure more directly the brain activity elicited by the inhibition of behaviour. Using event-related potentials in a simple Go–NoGo task, Malloy et al. (1989) reported that in OCD patients, the P300 component of the NoGo condition was located further anterior than the corresponding P300 of the Go condition. Furthermore, they found that the patients with OCD showed significantly decreased P300 amplitudes in the NoGo condition over frontal electrode positions as compared to healthy controls. This finding is in accordance with the reported inhibition deficit and the reduced frontal activity during rest in OCD. In contrast to this, Di Russo et al. (2000) reported differences between OCD and controls in the Go condition, with significantly higher P300 amplitudes for OCD in contrast to controls over the frontal cortex. The aim of the present study was to test whether OCD can be characterised by diminished or increased NoGo P300 amplitudes over the prefrontal cortex. We used topographical analyses of the ERP data because the anteriorisation of the positive brain electrical field during the NoGo condition is a very reliable and stable topographical descriptor of the main effects of the Go–NoGo task (Fallgatter et al., 2002, Fallgatter et al., 2001, Fallgatter et al., 2000). The hypothesis of this study is that OCD patients have a reduced P300 anteriorisation during the NoGo condition. As the N200 component is also discussed as an important component of Go–NoGo tasks (Falkenstein et al., 1999, Kiefer et al., 1998), we added analyses of the N200.

Section snippets

Subjects

Twelve patients (eight male, four female) from the inpatient and outpatient Department for Psychiatry and Psychotherapy at the University of Würzburg were recruited for this study. For the current study all patients gave their informed consent. All patients fulfilled the diagnosis of obsessive–compulsive disorder according to DSM-IV. Eleven patients had obsessions and compulsions, and one patient had mainly obsessions. All patients underwent a detailed psychiatric examination. They were

Behavioural data

The mean reaction times in the Go condition were 415.8±108.2 ms for patients and 500.0±129.3 ms for controls (t=1.73, P<0.10). Omission errors (missing reaction to Go) occurred on average 0.50±0.79 times for the patients and 0.50±0.91 times for the control group (t=0, n.s.). Commission errors (reactions in other conditions than the Go conditions) occurred on average 0.58±0.90 times for the patients and 0.58±1.00 times for the control group (t=0, n.s.).

EEG data

Conditions as well as groups differed

Discussion

As the main result of our study, we found topographical group differences in the brain electrical field of the NoGo condition, with patients showing a less pronounced anteriorisation of the P300 brain electrical field during inhibition as compared to controls, which was reflected by a diminished NGA in the patients. The N200 components, with more ‘negative’ values in the NoGo as compared to the Go condition, however, did not yield any significant group differences. In previous studies, the N200

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