S528 Abstracts mean correlation of each voxel to the overall brain and compared between groups over time. For this purpose, a flexible factorial design was used. The type of learning-task (group) and the scan number (time) were entered into the model as factors. Subjects were used as repeated-factors. Voxelwise FC was defined as the dependent variable. Results are reported after correction with family-wise error rate (FWER) at a peak ppeak ≤ 0.05 or cluster level pcluster ≤ 0.05 following an uncorrected threshold of p ≤ 0.001. Results: We found no significant interaction effect (group x time), though significant main effects of time could be shown in the left parahippocampus / superior temporal pole (ppeak=0.002), left supramarginal gyrus / superior temporal gyrus (pcluster=0.002, ppeak=0.008) and the left and the right premotor area / supplementary motor cortex (pcluster=0.010 (L) / 0.002 (R)). Post-hoc t-tests confirmed the increase of GFC at the 2nd measurement, for both paradigms. Conclusions: Our findings support the hypothesis that learning influences resting-state GFC across areas involved in learning, especially the parahippocampus and the tem- poral pole. These areas are found to be structurally and / or functionally altered in selected neuropsychiatric condi- tions, such as depression and anxiety disorders [4] or mild cognitive impairment [5]. Therefore, treatment-induced neuroplastic changes might be further investigated based on associative learning paradigms, presenting a valuable model for potential interactions of pharmacological agents (e.g., SSRIs) and learning in the course of multidimensional therapeutic approaches. Disclosure statement: R. Lanzenberger received con- ference speaker honorarium within the last three years from Shire and support from Siemens Healthcare regarding clinical research using PET/MR. He is shareholder of Brain Metabolics GmbH since Feb. 2019. M. Klöbl is a recipient of a DOC Fellowship of the Austrian Academy of Sciences. R. Seiger received funding from the Hochschuljubilaeumss- tiftung of the City of Vienna. References [1] Draganski, B., et al., 2004. Neuroplasticity: changes in grey matter induced by training. Nature 427 (6972), 311–312. [2] Holtmaat, A., Caroni, P., 2016. Functional and structural un- derpinnings of neuronal assembly formation in learning. Nat. Neurosci. 19 (12), 1553–1562. [3] Buckner, R.L., Vincent, J.L., 2007. Unrest at rest: default activ- ity and spontaneous network correlations. Neuroimage 37 (4), 1091–1096. [4] van Tol, M.J., et al., 2010. Regional brain volume in depres- sion and anxiety disorders. Arch. Gen. Psychiatry 67 (10), 1002– 1011. [5] Liu, J., et al., 2016. Impaired Parahippocampus Connectiv- ity in Mild Cognitive Impairment and Alzheimer’s Disease. J. Alzheimers Dis. 49 (4), 1051–1064. doi: 10.1016/j.euroneuro.2019.09.816 P.790 Adjunctive pregabalin in patients with major de- pressive disorder and enduring anxiety A. Hrnjica 1,∗ , S. Bise 2 , R. Setic 3 , I. Lokmic- Pekic 4 , G. Sulejmanpasic 5 1 Psychiatric hospital Sarajevo, Men’s department, Sara- jevo, Bosnia and Herzegovina 2 Psychiatric hospital Sarajevo, Women’s department, Sara- jevo, Bosnia and Herzegovina 3 Center for Mental Health Sarajevo, Psychology depart- ment, Sarajevo, Bosnia and Herzegovina 4 Psychiatric hospital Sarajevo, Intensive care department, Sarajevo, Bosnia and Herzegovina 5 Clinical center University of Sarajevo- Psychiatric clinic, Intensive care department, Sarajevo, Bosnia and Herzegov- ina Background: Anxiety symptoms in major depressive dis- order (MDD) result often in treatment resistance, residual symptoms, and persistent functional impairment. Antide- pressants (AD) are currently the mainstay of treatment both for depressive and for symptoms of anxiety. However, almost two-thirds of patients will fail to achieve remission with initial treatment, as a result, a range of augmentation and combination strategies have been used [1]. It has been suggested that pregabalin may be useful as add on therapy to AD in the treatment of anxiety in MDD. Pre- gabalin has a similar molecular structure to the inhibitory neurotransmitter gamma aminobutyric acid (GABA) but its mechanism of action does not appear to be mediated through effects on GABA. Instead, its anxiolytic effects may arise through high-affinity binding to the alpha-2-delta sub-unit of the P/Q type voltage-gated calcium channel in “over-excited” presynaptic neurons, thereby reducing the release of excitatory neurotransmitters such as glutamate [2]. It has been proven to show analgesic, anxiolytic, an- ticonvulsant and sleep enhancement effects, which could be applicable in the treatment of a variety of psychiatric disorders. Pregabalin could, in theory, have certain relative advan- tages, relating to the speed of onset of efficacy, the breadth of efficacy, and the absence of particular adverse effects seen during treatment with other medicaments (AD and benzodiazepines) in order to treat residual anxiety in MDD. Objective: The aim of the study was to evaluate tolerability and treatment outcomes associated with the adjunctive pregabalin to AD therapy for residual anxiety in patients with MDD. Methods: The study has involved 12 patients, all female; mean age 46.8 ± 13.55 years. Eligible patients were those diagnosed with MDD (based on DSM-V) with residual anxiety, not responding to previous therapy with AD. AD therapy has been ongoing for at least 4 weeks prior to the aug- mentation with pregabalin. The mean maximum pregabalin dose prescribed was 150 ± 67 mg (range, 150-300 mg/day). Therapeutical effects have been measured using Hamil- ton Anxiety Rating Scale (HAM-A), Hamilton Rating Scale for Depression- 17 items (HAM-D-17) and Clinical Global Impression- Severity of Illness and Global Improvement sub- scales (CGI-S and CGI-I). Adverse effects were monitored