Bipolar disorder (BPD) is often misdiagnosed as unipolar depression. This leads to inadequate treatment and can have negative impact on the course of the disease. There is now preliminary evidence that patients with unipolar and bipolar depression as well as healthy individuals with a heightened risk of BPD can be distinguished from each other based on their brain activity patterns and functional connectivity during resting state. However, the impact of pharmacological treatment on these functional brain measures have not yet been clarified. For common antidepressants it has been shown that they seem to normalise aberrant brain activity patterns and functional connectivity. The problem is that some antidepressants can induce mania or accelerate pathological cycling in depressive patients with unrecognised BPD. Therefore, pharmacological drugs with mood-stabilising properties such as quetiapine are more and more prescribed. Although the effectiveness and tolerability have been proven, the neuronal effects of these adjunctive treatments are not clear. The aim of the study is thus to investigate the impact of quetiapine on measures of brain activity in depressive patients with a heightened risk of BPD. Moreover, the investigators want to examine whether the investigators can distinguish depressive patients with a heightened risk of BPD from depressive patients without a heightened risk of BPD using neuroimaging techniques, and whether these measures can predict the course of the disease.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
DOUBLE
Enrollment
54
See information in arm description.
See information in arm description.
Clinic for psychiatry, psychotherapy and psychosomatic, RWTH Aachen University Hospital
Aachen, North Rhine-Westphalia, Germany
BOLD signal during a combined inhibition-reward-task
At baseline (day 0) the risk-group and control-group will be compared on BOLD signal (and behavioural data) during a combined inhibition-reward-task (neuronal correlate of cognitive control) (fMRI). These measures will be obtained once again at visit 4 (day 56) in the risk-group to evaluate the impact of quetiapine (i.e. change from baseline measure).
Time frame: Baseline (Day 0)
Functional connectivity in the default mode network during resting state (rstfMRI)
At baseline (day 0) the risk-group and control-group will be compared on functional connectivity in the default mode network during resting state (rstfMRI).
Time frame: Baseline (Day 0)
Structural differences in brain anatomy (MRI)
At baseline (day 0) the risk-group and control-group will be compared on structural differences in brain anatomy (MRI).
Time frame: Baseline (Day 0)
Structural integrity of nerve fibres (DTI)
At baseline (day 0) the risk-group and control-group will be compared on structural integrity of nerve fibres (DTI).
Time frame: Baseline (Day 0)
Effect of quetiapine on brain measures
After the quetiapine/ placebo intervention the risk-group will be compared whether there are changes from baseline in outcome measures 1 to 4.
Time frame: Visit 4 (Day 56)
Plasma levels of quetiapine
Blood samples of the patients of the risk group will be obtained to analyse the plasma levels of quetiapine.
Time frame: Visit 4 (Day 56)
Change over time in affect and psychopathology
All patients (risk-group and control group) will be assessed with questionnaires tapping affect and psychopathology (MADRS, YMRS, CGI, PANSS, BDI-II, Bf-S, SWN-K, EPS, BARS, C-SSRS, NGASR). These measures will be obtained at three different time points to evaluate the respective change over time.
Time frame: Baseline (Day 0), Visit 4 (Day 56), Follow-up (after 1 year)
Personality
All patients (risk-group and control group) will be assessed with questionnaires of personality (TCI-R, BIS-15, RS-13).
Time frame: Baseline (Day 0)
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