Andreas Heinz

Charité Universitätsmedizin Berlin, Berlín, Berlin, Germany

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Publications (667)2636.93 Total impact

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    ABSTRACT: Schizophrenia is a heterogeneous disorder that presents differently in men and women: men show a higher propensity to negative symptoms, lower social functioning, earlier age at onset and co-morbid substance abuse, whereas women display more affective symptoms. It is unknown whether these differences extend to subjects at high risk (HR) of psychosis. Thus, the aim of the present study was to address this question. Clinical symptoms and functioning were assessed using structured interviews in 239 HR subjects (female, n = 80). The definition of being at HR was based on the criteria used in the European Prediction of Psychosis Study (EPOS). Men displayed more pronounced negative symptoms, higher rates of past substance abuse disorders and higher deficits in social functioning. No gender difference was found for depression, which affected almost 50% of the cohort, or age at onset for the fulfilment of HR criteria. The higher impairment in specific symptoms observed in male schizophrenia patients was also present in subjects at HR for psychosis. Further studies are required to determine whether these symptoms are gender-specific predictors of transition to psychosis and whether they warrant gender-specific interventions. The high propensity to depression in the present cohort, which was particularly pronounced in the male cohort compared with the general population, in conjunction with the observed increase in negative symptoms and functional impairment, should alert clinicians to the necessity for the identification and treatment of HR subjects, irrespective of the degree to which these features are associated with transition risk. © 2015 Wiley Publishing Asia Pty Ltd.
    Early Intervention in Psychiatry 03/2015; DOI:10.1111/eip.12240 · 1.65 Impact Factor
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    ABSTRACT: Contemporary psychiatry is becoming more biologically oriented in the attempt to elicit a biological rationale of mental diseases. Although mental disorders comprise mostly functional abnormalities, there is a substantial overlap between neurology and psychiatry in addressing cognitive disturbances. In schizophrenia, the presence of cognitive impairment prior to the onset of psychosis and early after its manifestation suggests that some neurocognitive abnormalities precede the onset of psychosis and may represent a trait marker. These cognitive alterations may arise from functional disconnectivity, as no significant brain damage has been found. In this review we aim to revise A.R. Luria's systematic approach used in the neuropsychological evaluation of cognitive functions, which was primarily applied in patients with neurological disorders and in the cognitive evaluation in schizophrenia and other related disorders. As proposed by Luria, cognitive processes, associated with higher cortical functions, may represent functional systems that are not localized in narrow, circumscribed areas of the brain, but occur among groups of concertedly working brain structures, each of which makes its own particular contribution to the organization of the functional system. Current developments in neuroscience provide evidence of functional connectivity in the brain. Therefore, Luria's approach may serve as a frame of reference for the analysis and interpretation of cognitive functions in general and their abnormalities in schizophrenia in particular. Having said that, modern technology, as well as experimental evidence, may help us to understand the brain better and lead us towards creating a new classification of cognitive functions. In schizophrenia research, multidisciplinary approaches must be utilized to address specific cognitive alterations. The relationships among the components of cognitive functions derived from the functional connectivity of the brain may provide an insight into cognitive machinery.
    Philosophy Ethics and Humanities in Medicine 03/2015; DOI:10.1186/s13010-015-0026-9
  • 02/2015; 14(1). DOI:10.1002/wps.20182
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    ABSTRACT: Alcohol-dependent patients have been shown to faster approach than avoid alcohol stimuli on the Approach Avoidance Task (AAT). This so-called alcohol approach bias has been associated with increased brain activation in the medial prefrontal cortex and nucleus accumbens. Cognitive bias modification (CBM) has been used to retrain the approach bias with the clinically relevant effect of decreasing relapse rates one year later. The effects of CBM on neural signatures of approach/avoidance tendencies remain hitherto unknown. In a double-blind placebo-controlled design, 26 alcohol-dependent in-patients were assigned to a CBM or a placebo training group. Both groups performed the AAT for three weeks: in CBM training, patients pushed away 90 percent of alcohol cues; this rate was 50 percent in placebo training. Before and after training, patients performed the AAT offline, and in a 3 T magnetic resonance imaging scanner. The relevant neuroimaging contrast for the alcohol approach bias was the difference between approaching versus avoiding alcohol cues relative to soft drink cues: [(alcohol pull > alcohol push) > (soft drink pull > soft drink push)]. Before training, both groups showed significant alcohol approach bias-related activation in the medial prefrontal cortex. After training, patients in the CBM group showed stronger reductions in medial prefrontal cortex activation compared with the placebo group. Moreover, these reductions correlated with reductions in approach bias scores in the CBM group only. This suggests that CBM affects neural mechanisms involved in the automatic alcohol approach bias, which may be important for the clinical effectiveness of CBM.
    Addiction Biology 02/2015; DOI:10.1111/adb.12221 · 5.93 Impact Factor
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    ABSTRACT: The highly complex structure of the human brain is strongly shaped by genetic influences1. Subcortical brain regions form circuits with cortical areas to coordinate movement2, learning, memory3 and motivation4, and altered circuits can lead to abnormal behaviour and disease2. To investigate how common genetic variants affect the structure of these brain regions, here we conduct genome-wide association studies of the volumes of seven subcortical regions and the intracranial volume derived from magnetic resonance images of 30,717 individuals from 50 cohorts. We identify five novel genetic variants influencing the volumes of the putamen and caudate nucleus. We also find stronger evidence for three loci with previously established influences on hippocampal volume5 and intracranial volume6. These variants show specific volumetric effects on brain structures rather than global effects across structures. The strongest effects were found for the putamen, where a novel intergenic locus with replicable influence on volume (rs945270; P = 1.08 × 10−33; 0.52% variance explained) showed evidence of altering the expression of the KTN1 gene in both brain and blood tissue. Variants influencing putamen volume clustered near developmental genes that regulate apoptosis, axon guidance and vesicle transport. Identification of these genetic variants provides insight into the causes of variability in human brain development, and may help to determine mechanisms of neuropsychiatric dysfunction.
    Nature 01/2015; DOI:10.1038/nature14101 · 42.35 Impact Factor
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    ABSTRACT: Dual system theories suggest that behavioral control is parsed between a deliberative "model-based" and a more reflexive "model-free" system. A balance of control exerted by these systems is thought to be related to dopamine neurotransmission. However, in the absence of direct measures of human dopamine, it remains unknown whether this reflects a quantitative relation with dopamine either in the striatum or other brain areas. Using a sequential decision task performed during functional magnetic resonance imaging, combined with striatal measures of dopamine using [(18)F]DOPA positron emission tomography, we show that higher presynaptic ventral striatal dopamine levels were associated with a behavioral bias toward more model-based control. Higher presynaptic dopamine in ventral striatum was associated with greater coding of model-based signatures in lateral prefrontal cortex and diminished coding of model-free prediction errors in ventral striatum. Thus, interindividual variability in ventral striatal presynaptic dopamine reflects a balance in the behavioral expression and the neural signatures of model-free and model-based control. Our data provide a novel perspective on how alterations in presynaptic dopamine levels might be accompanied by a disruption of behavioral control as observed in aging or neuropsychiatric diseases such as schizophrenia and addiction.
    Proceedings of the National Academy of Sciences 01/2015; 112(5). DOI:10.1073/pnas.1417219112 · 9.81 Impact Factor
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    ABSTRACT: Ethnic minority groups show elevated suicide attempt rates across Europe. Evidence suggests a similar trend for women of Turkish origin in Germany, yet data on suicidal behaviour in minorities in Germany is scarce. The objective was to examine rates of suicidal behaviour, underlying motives, and to explore the effectiveness of an intervention program.
    European Psychiatry 01/2015; DOI:10.1016/j.eurpsy.2014.12.003 · 3.21 Impact Factor
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    ABSTRACT: Aggregation of functional magnetic resonance imaging (fMRI) data in regions-of-interest (ROI) is required for complex statistical analyses not implemented in standard fMRI software. Different data-aggregation methods assess various aspects of neural activation, including spatial extent and intensity. New method: In this study, conducted within the framework of the PREDICT study, we compared different aggregation measures for voxel-wise fMRI activations to be used as prognostic factors for relapse in 49 abstinent alcohol-dependent individuals in an outpatient setting using a cue-reactivity task. We compared the importance of the data-aggregation measures as prognostic factors for treatment outcomes by calculating the proportion of explained variation. Results and comparison with existing method(s): Relapse risk was associated with cue-induced brain activation during abstinence in the ventral striatum (VS) and in the orbitofrontal cortex (OFC). While various ROI measures proved appropriate for using fMRI cue-reactivity to predict relapse, on the descriptive level the most "important" prognostic factor was a measure defined as the sum of t-values exceeding an individually defined threshold. Data collected in the VS was superior to that from other regions. In conclusion, it seems that fMRI cue-reactivity, especially in the VS, can be used as prognostic factor for relapse in abstinent alcohol-dependent patients. Our findings suggest that data-aggregation methods that take both spatial extent and intensity of cue-induced brain activation into account make better biomarkers for predicting relapse than methods that consider an activation's spatial extent or intensity alone. NCT00317031. Copyright © 2015. Published by Elsevier B.V.
    Journal of Neuroscience Methods 01/2015; DOI:10.1016/j.jneumeth.2015.01.001 · 1.96 Impact Factor
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    ABSTRACT: Changes in reward processing have been identified as one important pathogenetic mechanism in alcohol addiction. The nonsynonymous single nucleotide polymorphism in the brain-derived neurotrophic factor (BDNF) gene (rs6265/Val66Met) modulates the central nervous system activity of neurotransmitters involved in reward processing such as serotonin, dopamine, and glutamate. It was identified as crucial for alcohol consumption in healthy adults and, in rats, specifically related to the function in the striatum, a region that is commonly involved in reward processing. However, studies in humans on the association of BDNF Val66Met and reward-related brain functions and its role for alcohol consumption, a significant predictor of later alcohol addiction, are missing. Based on an intermediate phenotype approach, we assessed the early orientation toward alcohol and alcohol consumption in 530 healthy adolescents that underwent a monetary incentive delay task during functional magnetic resonance imaging. We found a significantly lower response in the putamen to reward anticipation in adolescent Met carriers with high versus low levels of alcohol consumption. During reward feedback, Met carriers with low putamen reactivity were significantly more likely to orient toward alcohol and to drink alcohol 2 years later. This study indicates a possible effect of BDNF Val66Met on alcohol addiction-related phenotypes in adolescence.
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    ABSTRACT: Functional neuroimaging has provided evidence for altered function of mesolimbic circuits implicated in reward processing, first and foremost the ventral striatum, in patients with schizophrenia. While such findings based on significant group differences in brain activations can provide important insights into the pathomechanisms of mental disorders, the use of neuroimaging results from standard univariate statistical analysis for individual diagnosis has proven difficult. In this proof of concept study, we tested whether the predictive accuracy for the diagnostic classification of schizophrenia patients vs. healthy controls could be improved using multivariate pattern analysis (MVPA) of regional functional magnetic resonance imaging (fMRI) activation patterns for the anticipation of monetary reward. With a searchlight MVPA approach using support vector machine classification, we found that the diagnostic category could be predicted from local activation patterns in frontal, temporal, occipital and midbrain regions, with a maximal cluster peak classification accuracy of 93% for the right pallidum. Region-of-interest based MVPA for the ventral striatum achieved a maximal cluster peak accuracy of 88%, whereas the classification accuracy on the basis of standard univariate analysis reached only 75%. Moreover, using support vector regression we could additionally predict the severity of negative symptoms from ventral striatal activation patterns. These results show that MVPA can be used to substantially increase the accuracy of diagnostic classification on the basis of task-related fMRI signal patterns in a regionally specific way.
    PLoS ONE 01/2015; 10(3):e0119089. DOI:10.1371/journal.pone.0119089 · 3.53 Impact Factor
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    ABSTRACT: Objective: In alcohol-dependent patients, alcohol cues evoke increased activation in mesolimbic brain areas, such as the nucleus accumbens and the amygdala. Moreover, patients show an alcohol approach bias, a tendency to more quickly approach than avoid alcohol cues. Cognitive bias modification training, which aims to retrain approach biases, has been shown to reduce alcohol craving and relapse rates. The authors investigated effects of this training on cue reactivity in alcohol-dependent patients. Method: In a double-blind randomized design, 32 abstinent alcohol-dependent patients received either bias modification training or sham training. Both trainings consisted of six sessions of the joystick approach-avoidance task; the bias modification training entailed pushing away 90% of alcohol cues and 10% of soft drink cues, whereas this ratio was 50/50 in the sham training. Alcohol cue reactivity was measured with functional MRI before and after training. Results: Before training, alcohol cue-evoked activation was observed in the amygdala bilaterally, as well as in the right nucleus accumbens, although here it fell short of significance. Activation in the amygdala correlated with craving and arousal ratings of alcohol stimuli; correlations in the nucleus accumbens again fell short of significance. After training, the bias modification group showed greater reductions in cue-evoked activation in the amygdala bilaterally and in behavioral arousal ratings of alcohol pictures, compared with the sham training group. Decreases in right amygdala activity correlated with decreases in craving in the bias modification but not the sham training group. Conclusions: These findings provide evidence that cognitive bias modification affects alcohol cue-induced mesolimbic brain activity. Reductions in neural reactivity may be a key underlying mechanism of the therapeutic effectiveness of this training.
    American Journal of Psychiatry 12/2014; DOI:10.1176/appi.ajp.2014.13111495 · 13.56 Impact Factor
  • A Heinz
    Der Nervenarzt 12/2014; DOI:10.1007/s00115-014-4068-9 · 0.86 Impact Factor
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    ABSTRACT: Theories of decision-making and its neural substrates have long assumed the existence of two distinct and competing valuation systems, variously described as goal-directed vs. habitual, or, more recently and based on statistical arguments, as model-free vs. model-based reinforcement-learning. Though both have been shown to control choices, the cognitive abilities associated with these systems are under ongoing investigation. Here we examine the link to cognitive abilities, and find that individual differences in processing speed covary with a shift from model-free to model-based choice control in the presence of above-average working memory function. This suggests shared cognitive and neural processes; provides a bridge between literatures on intelligence and valuation; and may guide the development of process models of different valuation components. Furthermore, it provides a rationale for individual differences in the tendency to deploy valuation systems, which may be important for understanding the manifold neuropsychiatric diseases associated with malfunctions of valuation.
    Frontiers in Psychology 12/2014; 5:1450. DOI:10.3389/fpsyg.2014.01450 · 2.80 Impact Factor
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    ABSTRACT: Hippocampal dysfunction and deficits in episodic memory have been reported for both Alzheimer’s disease (AD) and major depressive disorder (MDD). Primacy performance has been associated with hippocampus-dependent episodic memory, while recency may reflect working memory performance. In this study, serial position profiles were examined in a total of 73 patients with MDD, AD, both AD and MDD, and healthy controls (HC) by means of CERAD-NP word list memory. Primacy performance was most impaired in AD with comorbid MDD, followed by AD, MDD, and HC. Recency performance, on the other hand, was comparable across groups. These findings indicate that primacy in AD is impaired in the presence of comorbid MDD, suggesting additive performance decrements in this specific episodic memory function.
    12/2014; 27(4). DOI:10.1024/1662-9647/a000115
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    ABSTRACT: Previous research on alcohol dependent patients has shown that variations in eyeblink startle response can be used as an indicator of their emotional responses to alcohol-related stimuli. Postulating that reactions on substance associated stimuli are controlled by either a negative or a positive affective processing system, we expect that abstinent alcoholics react differently (within-group) in the emotional evaluation of alcohol cues. Furthermore, we assumed the startle response to covary with medication response to acamprosate and naltrexone. We measured 74 detoxified inpatients' acoustic startle responses while they were being presented with alcohol-related images as well as affectively negative, neutral, and positive pictures before they were randomized to pharmacotherapy. Group-mean startle peak amplitudes were lowest for alcohol-related cues. The relative startle response (alcohol cues set in relation to the other stimulus categories) did not correlate with craving for alcohol (OCDS) or alcohol cue induced self-ratings of arousal, valence and craving. Patients with a lower percentage of abstinent days in the 90days prior to the last drinking day showed a lower ("more appetitive") startle response to alcohol cues. A survival analysis using the time to first heavy drinking day as the survival criterion revealed a significant interaction between alcohol-cue startle responses and medication type. The results indicate that the psycho-physiological measure of emotional evaluation of alcohol cues includes unconscious processing not reflected by conscious self-ratings. Furthermore, our result of a differential medication effect may encourage further studies to use biological characteristics to stratify patients as a step towards individualized treatment for alcohol dependence.
    International journal of psychophysiology: official journal of the International Organization of Psychophysiology 12/2014; 94(3):263-71. DOI:10.1016/j.ijpsycho.2014.09.009 · 3.05 Impact Factor
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    ABSTRACT: Drugs of abuse elicit dopamine release in the ventral striatum, possibly biasing dopamine-driven reinforcement learning towards drug-related reward at the expense of non-drug-related reward. Indeed, in alcohol-dependent patients, reactivity in dopaminergic target areas is shifted from non-drug-related stimuli towards drug-related stimuli. Such ‘hijacked’ dopamine signals may impair flexible learning from non-drug-related rewards, and thus promote craving for the drug of abuse. Here, we used functional magnetic resonance imaging to measure ventral striatal activation by reward prediction errors (RPEs) during a probabilistic reversal learning task in recently detoxified alcohol-dependent patients and healthy controls (N = 27). All participants also underwent 6-[18F]fluoro-DOPA positron emission tomography to assess ventral striatal dopamine synthesis capacity. Neither ventral striatal activation by RPEs nor striatal dopamine synthesis capacity differed between groups. However, ventral striatal coding of RPEs correlated inversely with craving in patients. Furthermore, we found a negative correlation between ventral striatal coding of RPEs and dopamine synthesis capacity in healthy controls, but not in alcohol-dependent patients. Moderator analyses showed that the magnitude of the association between dopamine synthesis capacity and RPE coding depended on the amount of chronic, habitual alcohol intake. Despite the relatively small sample size, a power analysis supports the reported results. Using a multimodal imaging approach, this study suggests that dopaminergic modulation of neural learning signals is disrupted in alcohol dependence in proportion to long-term alcohol intake of patients. Alcohol intake may perpetuate itself by interfering with dopaminergic modulation of neural learning signals in the ventral striatum, thus increasing craving for habitual drug intake.
    European Journal of Neuroscience 12/2014; 41(4). DOI:10.1111/ejn.12802 · 3.67 Impact Factor
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    ABSTRACT: Chronic drug intake (including alcohol) has profound neurotoxic and neuroadaptive consequences on neurotransmitter systems and brain circuitries that are strongly involved in learning and memory. Neuroadaptive alterations within these systems can contribute to addiction development and maintenance. Current brain-imaging studies identified neural correlates of behavioral processes that play a key role in addiction, such as cue-induced craving or automatic action tendencies. Such neurobiological findings reflect neuroadaptations to chronic drug intake, to further environmental as well as genetic factors and serve as dispositional factors for the maintenance of addictive behavior patterns. In this chapter, we describe neurobiological theories of addiction development and maintenance with a focus on motivational alterations and their neurobiological correlates as revealed by current neuroimaging studies in alcohol dependence. We discuss findings that assess alterations in reward anticipation and processing and their respective effects on learning mechanisms that are known to be implied in alcohol dependence. A better understanding of neural processes directly associated with the development and maintenance of addiction can help to improve prevention programs as well as therapeutic and specifically pharmacological interventions in the treatment of addicted patients.
    Textbook of Addiction Treatment: International Perspectives, Edited by Nady el-Guebaly, Giuseppe Carrà, Marc Galanter, 11/2014: pages 9-38;
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    ABSTRACT: Approximately 20–30% of patients with Major depressive disorder (MDD) develop a chronic course of their disease. Chronic depression is associated with increased health care utilisation, hospitalisation and a higher disease burden. We identified clinical correlates and differences in treatment response of chronic MDD (cMDD) patients compared with non-chronic episodic depression in a huge sample of depressive inpatients.Methods Data were collected from 412 inpatients who had been diagnosed with a major depressive episode (MDE; according to ICD-10) and scored 15 or higher on the 21-item Hamilton Depression Rating Scale (HRSD-21). All subjects were participants in the German Algorithm Project, phase 3 (GAP3). Patients who were diagnosed with a MDE within the last two years or longer (herein referred to as CD) were compared with non-chronic depressive patients (herein referred to as non-CD). CD and non-CD patients were assessed for the following: psychosocial characteristics, symptom reduction from hospital admission to discharge, symptom severity at discharge, remission and response rates, and pharmacological treatment during inpatient treatment. The primary outcome measure was the HRSD-21.Results13.6% (n=56) of patients met the criteria for chronic depression. Compared with non-CD patients, patients with CD showed increased axis I comorbidities (74% vs. 52%, χ2 (1)=7.31, p=.02), a higher level of depressive symptoms at baseline and discharge, increased duration of inpatient treatment (64.8 vs. 53.3 days; t=2.86, p=.03) and lower response (HRSD: 60.0% vs. 72.0%; χ2 (1)=3.61, p<.04; BDI: 40.5% vs. 54.2%; χ2 (1)=3.56, p=.04) and remission rates (BDI 17.9.% vs. 29.7%; χ2 (1)=3.42, p=.05. However, both groups achieved a comparable symptom reduction during inpatient treatment. The prescribed pharmacological strategy had no significant influence on treatment outcome in patients with CD.Conclusion Inpatients with CD show higher symptom severity, lower response and remission rates and a longer duration of inpatient treatment, although they achieve comparable symptom reduction during treatment. These findings support the need to recognise CD and its defining characteristics as a distinct subclass of depression.
    Journal of Affective Disorders 11/2014; DOI:10.1016/j.jad.2014.10.059 · 3.71 Impact Factor

Publication Stats

13k Citations
2,636.93 Total Impact Points


  • 2002–2015
    • Charité Universitätsmedizin Berlin
      • • Department of Psychiatry and Psychotherapy
      • • Department of Psychiatry
      Berlín, Berlin, Germany
  • 2002–2014
    • Humboldt-Universität zu Berlin
      • Department of Psychology
      Berlín, Berlin, Germany
  • 2013
    • University of Greifswald
      Griefswald, Mecklenburg-Vorpommern, Germany
    • Technische Universität Dresden
      Dresden, Saxony, Germany
  • 2000–2013
    • Central Institute of Mental Health
      • Klinik für Abhängiges Verhalten und Suchtmedizin
      Mannheim, Baden-Wuerttemberg, Germany
    • National Institute on Alcohol Abuse and Alcoholism
      Maryland, United States
  • 2012
    • Kliniken Essen-Mitte Knappschafts-Krankenhaus
      Essen, North Rhine-Westphalia, Germany
    • Bernstein Center for Computational Neuroscience Berlin
      Berlín, Berlin, Germany
  • 2008–2012
    • King's College London
      • Institute of Psychiatry
      London, ENG, United Kingdom
    • Max Planck Institute of Psychiatry
      München, Bavaria, Germany
    • Aarhus University
      • Centre of Functionally Integrative Neuroscience CFIN
      Aars, Region North Jutland, Denmark
    • Johannes Gutenberg-Universität Mainz
      • Klinik und Poliklinik für Psychosomatische Medizin und Psychotherapie
      Mainz, Rhineland-Palatinate, Germany
  • 2011
    • University of Toronto
      • Rotman Research Institute
      Toronto, Ontario, Canada
    • University of Illinois at Chicago
      • Department of Psychology
      Chicago, Illinois, United States
  • 2010–2011
    • University of Cologne
      • Department of Psychiatry and Psychotherapy
      Köln, North Rhine-Westphalia, Germany
  • 2001–2010
    • Universität Heidelberg
      • Central Institute of Mental Health
      Heidelburg, Baden-Württemberg, Germany
    • Royal Prince Alfred Hospital
      Camperdown, New South Wales, Australia
    • Hannover Medical School
      Hanover, Lower Saxony, Germany
  • 1990–2010
    • Ruhr-Universität Bochum
      • Neurologische Klinik
      Bochum, North Rhine-Westphalia, Germany
  • 2007
    • Queen Mary, University of London
      • Barts and The London School of Medicine and Dentistry
      London, ENG, United Kingdom
  • 2006
    • Universität Mannheim
      Mannheim, Baden-Württemberg, Germany
  • 2004–2005
    • University of Hamburg
      Hamburg, Hamburg, Germany
    • Bielefeld University
      Bielefeld, North Rhine-Westphalia, Germany
  • 2001–2005
    • University of Tuebingen
      Tübingen, Baden-Württemberg, Germany
  • 1996–1999
    • National Institute of Mental Health (NIMH)
      • Clinical Brain Disorders Branch
      Bethesda, MD, United States
  • 1994–1998
    • Freie Universität Berlin
      • Department of Psychiatry
      Berlín, Berlin, Germany
  • 1995
    • St. Josef-Hospital
      Bonn, North Rhine-Westphalia, Germany