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Delmenhorst, Germany

Staniloiu A.,Bielefeld University | Staniloiu A.,Hanse Institute for Advanced Study | Markowitsch H.J.,Bielefeld University
The Lancet Psychiatry | Year: 2014

Dissociative amnesia is one of the most enigmatic and controversial psychiatric disorders. In the past two decades, interest in the understanding of its pathophysiology has surged. In this report, we review new data about the epidemiology, neurobiology, and neuroimaging of dissociative amnesia and show how advances in memory research and neurobiology of dissociation inform proposed pathogenetic models of the disorder. Dissociative amnesia is characterised by functional impairment. Additionally, preliminary data suggest that affected people have an increased and possibly underestimated suicide risk. The prevalence of dissociative amnesia differs substantially across countries and populations. Symptoms and disease course also vary, indicating a possibly heterogeneous disorder. The accompanying clinical features differ across cultural groups. Most dissociative amnesias are retrograde, with memory impairments mainly involving the episodic-autobiographical memory domain. Anterograde dissociative amnesia occurring without significant retrograde memory impairments is rare. Functional neuroimaging studies of dissociative amnesia with prevailing retrograde memory impairments show changes in the network that subserves autobiographical memory. At present, no evidence-based treatments are available for dissociative amnesia and no broad framework exists for its rehabilitation. Further research is needed into its neurobiology, course, treatment options, and strategies to improve differential diagnoses. © 2014 Elsevier Ltd.

Taubner S.,Hanse Institute for Advanced Study | Taubner S.,Klagenfurt University | Wiswede D.,Hanse Institute for Advanced Study | Wiswede D.,University of Lubeck | And 2 more authors.
Frontiers in Human Neuroscience | Year: 2013

Objective: The heterogeneity between patients with depression cannot be captured adequately with existing descriptive systems of diagnosis and neurobiological models of depression. Furthermore, considering the highly individual nature of depression, the application of general stimuli in past research efforts may not capture the essence of the disorder. This study aims to identify subtypes of depression by using empirically derived personality syndromes, and to explore neural correlates of the derived personality syndromes. Materials and Methods: In the present exploratory study, an individually tailored and psychodynamically based functional magnetic resonance imaging paradigm using dysfunctional relationship patterns was presented to 20 chronically depressed patients. Results from the Shedler-Westen Assessment Procedure (SWAP-200) were analyzed by Q-factor analysis to identify clinically relevant subgroups of depression and related brain activation. Results: The principle component analysis of SWAP-200 items from all 20 patients lead to a two-factor solution: "wDepressive Personality" and "Emotional-Hostile-Externalizing Personality." Both factors were used in a whole-brain correlational analysis but only the second factor yielded significant positive correlations in four regions: a large cluster in the right orbitofrontal cortex (OFC), the left ventral striatum, a small cluster in the left temporal pole, and another small cluster in the right middle frontal gyrus. Discussion: The degree to which patients with depression score high on the factor "Emotional-Hostile-Externalizing Personality" correlated with relatively higher activity in three key areas involved in emotion processing, evaluation of reward/punishment, negative cognitions, depressive pathology, and social knowledge (OFC, ventral striatum, temporal pole). Results may contribute to an alternative description of neural correlates of depression showing differential brain activation dependent on the extent of specific personality syndromes in depression. © 2013 Taubner, Wiswede and Kessler.

Kessler H.,Hanse Institute for Advanced Study | Kessler H.,University of Ulm | Kessler H.,University of Bonn | Taubner S.,Hanse Institute for Advanced Study | And 13 more authors.
PLoS ONE | Year: 2011

Objectives: In the search for neurobiological correlates of depression, a major finding is hyperactivity in limbic-paralimbic regions. However, results so far have been inconsistent, and the stimuli used are often unspecific to depression. This study explored hemodynamic responses of the brain in patients with depression while processing individualized and clinically derived stimuli. Methods: Eighteen unmedicated patients with recurrent major depressive disorder and 17 never-depressed control subjects took part in standardized clinical interviews from which individualized formulations of core interpersonal dysfunction were derived. In the patient group such formulations reflected core themes relating to the onset and maintenance of depression. In controls, formulations reflected a major source of distress. This material was thereafter presented to subjects during functional magnetic resonance imaging (fMRI) assessment. Results: Increased hemodynamic responses in the anterior cingulate cortex, medial frontal gyrus, fusiform gyrus and occipital lobe were observed in both patients and controls when viewing individualized stimuli. Relative to control subjects, patients with depression showed increased hemodynamic responses in limbic-paralimbic and subcortical regions (e.g. amygdala and basal ganglia) but no signal decrease in prefrontal regions. Conclusions: This study provides the first evidence that individualized stimuli derived from standardized clinical interviewing can lead to hemodynamic responses in regions associated with self-referential and emotional processing in both groups and limbic-paralimbic and subcortical structures in individuals with depression. Although the regions with increased responses in patients have been previously reported, this study enhances the ecological value of fMRI findings by applying stimuli that are of personal relevance to each individual's depression. © 2011 Kessler et al.

Wiswede D.,University of Lubeck | Wiswede D.,Hanse Institute for Advanced Study | Taubner S.,Klagenfurt University | Taubner S.,Hanse Institute for Advanced Study | And 12 more authors.
PLoS ONE | Year: 2014

Objective: Neurobiological models of depression posit limbic hyperactivity that should normalize after successful treatment. For psychotherapy, though, brain changes in patients with depression show substantial variability. Two critical issues in relevant studies concern the use of unspecific stimulation experiments and relatively short treatment protocols. Therefore changes in brain reactions to individualized stimuli were studied in patients with depression after eight months of psychodynamic psychotherapy.Methods: 18 unmedicated patients with recurrent major depressive disorder were confronted with individualized and clinically derived content in a functional MRI experiment before (T1) and after eight months (T2) of psychodynamic therapy. A control group of 17 healthy subjects was also tested twice without intervention. The experimental stimuli were sentences describing each participant's dysfunctional interpersonal relationship patterns derived from clinical interviews based on Operationalized Psychodynamic Diagnostics (OPD).Results: At T1 patients showed enhanced activation compared to controls in several limbic and subcortical regions, including amygdala and basal ganglia, when confronted with OPD sentences. At T2 the differences in brain activity between patients and controls were no longer apparent. Concurrently, patients had improved significantly in depression scores.Conclusions: Using ecologically valid stimuli, this study supports the model of limbic hyperactivity in depression that normalizes after treatment. Without a control group of untreated patients measured twice, though, changes in patients' brain activity could also be attributed to other factors than psychodynamic therapy. © 2014 Wiswede et al.

Buchheim A.,University of Innsbruck | Viviani R.,University of Innsbruck | Viviani R.,University of Ulm | Kessler H.,Hanse Institute for Advanced Study | And 12 more authors.
PLoS ONE | Year: 2012

Neuroimaging studies of depression have demonstrated treatment-specific changes involving the limbic system and regulatory regions in the prefrontal cortex. While these studies have examined the effect of short-term, interpersonal or cognitive-behavioural psychotherapy, the effect of long-term, psychodynamic intervention has never been assessed. Here, we investigated recurrently depressed (DSM-IV) unmedicated outpatients (N = 16) and control participants matched for sex, age, and education (N = 17) before and after 15 months of psychodynamic psychotherapy. Participants were scanned at two time points, during which presentations of attachment-related scenes with neutral descriptions alternated with descriptions containing personal core sentences previously extracted from an attachment interview. Outcome measure was the interaction of the signal difference between personal and neutral presentations with group and time, and its association with symptom improvement during therapy. Signal associated with processing personalized attachment material varied in patients from baseline to endpoint, but not in healthy controls. Patients showed a higher activation in the left anterior hippocampus/amygdala, subgenual cingulate, and medial prefrontal cortex before treatment and a reduction in these areas after 15 months. This reduction was associated with improvement in depressiveness specifically, and in the medial prefrontal cortex with symptom improvement more generally. This is the first study documenting neurobiological changes in circuits implicated in emotional reactivity and control after long-term psychodynamic psychotherapy. © 2012 Buchheim et al.

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