One alternative explanation could be neural habituation effects as described in social anxiety disorders. It has been shown that stimulation through WZ8040 individualized pictures for the purpose of symptom provocation results in effects distinctly different from neutral, but also from standardized disgust-eliciting pictures. There are other studies that have investigated the results of individualized, system-provoking material, such as pictures from patients’personal environment, verbal descriptions of compulsion-related objects, or tactile stimulation through “dirty” objects. Buchheim et al. used individualized scripts of attachment-relevant themes, which were used to provoke attachment-relevant conflict patterns in repeated fMRI scans during the psychoanalytic process of treating chronically depressed patients. By investigating the role of corticoamygdala circuits in the pathophysiology of OCD, Simon et al. collected a great variety of symptom R428 Axl inhibitor triggers, where patients, in addition to exposure to standardized aversive and neutral pictures, were supposed to provide responses according to the degree of induced obsessive states, anxiety, valence and arousal. Meanwhile, the Maudsley Obsessive-Compulsive Stimuli Set provides a specific and standardized paradigm for symptom-specific provocation of OCD states, which in future could enable the application of individual and standardized pictures to be used in a combined paradigm. Several of the ROIs investigated in this study are part of a comprehensive OCD-related neuronal network and have been identified as change-relevant in a number of outcome studies on the psychotherapy of OCD. For the purpose of quantifying changes, rather large ROIs were selected, which made it impossible to focus on smaller basal ganglia structures, or areas of the amygdala. Other brain regions that have been related to OCD symptoms before did not show reliable responses in the present study, for example the ventromedial and the orbitofrontal cortex. The dimension of poor versus good insight could interfere with the results since there seem to exist neuronal correlates of different insight levels. Although patients were classified to the good insight level by their psychiatrists we did not apply a systematic measure of the poor vs. good insight dimension, since studies showed that the degree of insight did not predict the likelihood of response to psychotherapy. This and other possible therapy modulating covariates will be included in a replication study, which offers the possibility to take into consideration the shortcomings of this study. The replication of the study will include a larger sample size and another drug-free diagnostic group in addition to a healthy control group in order to distinguish between OCD-specific activation patterns on the one hand, and diagnosisindependent neuronal mechanisms during therapeutic change processes on the other hand. Furthermore, it would be interesting to perform the scans precisely during periods of low and high dynamic complexity and then compare order transitions with non order transitions as well as phases of critical instability with phases of relative stability. This comparison would be of great theoretical and clinical importance because critical instabilities represent the sensitive phases of therapies. The question would be whether neuronal correlates of instability during therapeutic change processes could be identified. This kind of investigation could focus on the cingulate cortex, which plays an important role as conflict monitoring system. Especially the dorsal part of the ACC is sensitive to ambiguous or conflicting information, is involved in decision making, and its activation is predictive to treatment outcome in depression.