Obsessive-compulsive disorder (OCD) is a common neuropsychiatric disorder marked by recurrent intrusive thoughts (obsessions) and repetitive behaviours (compulsions) with a prevalence of 2-3% (Karno et al., 1988). Neuroimaging studies provide evidence for the involvement of cortico-striatal circuits in OCD pathophysiology

OBJECTIVE: The goal of this study was to assess the activity of intracortical EEG sources in patients with OCD. METHODS: We compared resting state EEG from 50 OCD patients and 50 matched controls using standardized low-resolution electromagnetic tomography (sLORETA) and normative independent component analysis (NICA). Data were analyzed with 1 Hz frequency resolution. Group ICA was used to separate 7 independent components from the control group data. The resulting weights and norms served to derive the same components from the OCD group and to compare their power with controls. RESULTS: In OCD, sLORETA indicated low-frequency power excess (2 – 6 Hz) in the medial frontal cortex, whereas group ICA showed increased low-frequency power in a component reflecting the activity of subgenual anterior cingulate, adjacent limbic structures and to a lesser extent also of lateral frontal cortex. CONCLUSIONS: Both methods provided evidence for medial frontal hyperactivation in OCD. SIGNIFICANCE: Our study is the first to use normative ICA in a clinical sample and indicates its potential utility as a diagnostic tool. The findings provide consistent results based on EEG source localization in OCD and are of practical interest for therapeutic interventions. INTRODUCTION Obsessive-compulsive disorder (OCD) is a common neuropsychiatric disorder marked by recurrent intrusive thoughts (obsessions) and repetitive behaviours (compulsions) with a prevalence of 2-3% (Karno et al., 1988). Neuroimaging studies provide evidence for the involvement of cortico-striatal circuits in OCD pathophysiology (Aouizerate et al., 2004). The traditional and most widely accepted model, supported by a large body of scientific evidence, postulates a hyperactive orbitofronto-striatal circuit including orbitofrontal and cingulate cortex, ventral striatum, ventral pallidum, mediodorsal thalamus, hippocampus and amygdala (Menzies et al., 2008a). However, accumulating evidence from various methodological approaches suggests that OCD is mediated by more widely distributed neural networks including also dorsal brain regions such as dorsolateral prefrontal cortex (Gu et al., 2008; Remijnse et al., 2006; van den Heuvel et al., 2005), parietal cortex (Menzies et al., 2008b) or cerebellum (Nabeyama et al., 2008; van den Heuvel et al., 2009). A recent multimodal review and meta-analytic study by Menzies et al. (2008a) proposed a more comprehensive OCD model including two relatively segregated fronto-striatal networks: affective orbitofronto-striatal loop and dorsolateral prefrontostriatal loop which also includes parietal and lateral prefrontal cortex and subserves spatial and attentional functions. Aberrant functioning and imbalanced interactions between frontostriatal networks might explain clinical OCD symptoms and neuropsychological deficits such as excessive perception of error (Ullsperger and von Cramon, 2006), abnormal reward processing (Remijnse et al., 2006), cognitive and behavioural inflexibility (Gu et al., 2008) and difficulty to inhibit prepotent responses (Roth et al., 2007). Electroencephalographic (EEG) studies based on quantitative analysis reported abnormalities registered at frontal or frontotemporal electrode sites in OCD (e.g. Karadag et al., 2003; Pogarell et al., 2006; Prichep et al., 1993). However, only limited attention has been paid to the localization of generators of the aberrant EEG activity in OCD. EEG sources have been investigated in relation to treatment response (Bolwig et al., 2007; Fontenelle et al., 2006) and in subjects with obsessive-compulsive symptoms (Sherlin and Congedo, 2005) and recently also in drug naïve obsessive-compulsive patients (Velikova et al., 2010). All studies using lowha l-0 06 20 68 7, v er si on 1 8 Se p 20 11 Author manuscript, published in "Clinical Neurophysiology 122, 9 (2011) 1735-1743"