@misc{HaegeleSchlagenhaufRappetal.2014, author = {H{\"a}gele, Claudia and Schlagenhauf, Florian and Rapp, Michael Armin and Sterzer, Philipp and Beck, Anne and Bermpohl, Felix and Stoy, Meline and Str{\"o}hle, Andreas and Wittchen, Hans-Ulrich and Dolan, Raymond J. and Heinz, Andreas}, title = {Dimensional psychiatry}, series = {Postprints der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe}, journal = {Postprints der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe}, number = {653}, issn = {1866-8364}, doi = {10.25932/publishup-43106}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-431064}, pages = {331 -- 341}, year = {2014}, abstract = {A dimensional approach in psychiatry aims to identify core mechanisms of mental disorders across nosological boundaries. We compared anticipation of reward between major psychiatric disorders, and investigated whether reward anticipation is impaired in several mental disorders and whether there is a common psychopathological correlate (negative mood) of such an impairment. We used functional magnetic resonance imaging (fMRI) and a monetary incentive delay (MID) task to study the functional correlates of reward anticipation across major psychiatric disorders in 184 subjects, with the diagnoses of alcohol dependence (n = 26), schizophrenia (n = 44), major depressive disorder (MDD, n = 24), bipolar disorder (acute manic episode, n = 13), attention deficit/hyperactivity disorder (ADHD, n = 23), and healthy controls (n = 54). Subjects' individual Beck Depression Inventory-and State-Trait Anxiety Inventory-scores were correlated with clusters showing significant activation during reward anticipation. During reward anticipation, we observed significant group differences in ventral striatal (VS) activation: patients with schizophrenia, alcohol dependence, and major depression showed significantly less ventral striatal activation compared to healthy controls. Depressive symptoms correlated with dysfunction in reward anticipation regardless of diagnostic entity. There was no significant correlation between anxiety symptoms and VS functional activation. Our findings demonstrate a neurobiological dysfunction related to reward prediction that transcended disorder categories and was related to measures of depressed mood. The findings underline the potential of a dimensional approach in psychiatry and strengthen the hypothesis that neurobiological research in psychiatric disorders can be targeted at core mechanisms that are likely to be implicated in a range of clinical entities.}, language = {en} } @article{HeinzelRappFydrichetal.2017, author = {Heinzel, Stephan and Rapp, Michael Armin and Fydrich, Thomas and Str{\"o}hle, Andreas and Teran, Christina and Kallies, Gunnar and Schwefel, Melanie and Heissel, Andreas}, title = {Neurobiological mechanisms of exercise and psychotherapy in depression}, series = {Clinical Trials}, volume = {15}, journal = {Clinical Trials}, number = {1}, publisher = {Sage Publ.}, address = {London}, issn = {1740-7745}, doi = {10.1177/1740774517729161}, pages = {53 -- 64}, year = {2017}, abstract = {Background/Aims: Even though cognitive behavioral therapy has become a relatively effective treatment for major depressive disorder and cognitive behavioral therapy-related changes of dysfunctional neural activations were shown in recent studies, remission rates still remain at an insufficient level. Therefore, the implementation of effective augmentation strategies is needed. In recent meta-analyses, exercise therapy (especially endurance exercise) was reported to be an effective intervention in major depressive disorder. Despite these findings, underlying mechanisms of the antidepressant effect of exercise especially in combination with cognitive behavioral therapy have rarely been studied to date and an investigation of its neural underpinnings is lacking. A better understanding of the psychological and neural mechanisms of exercise and cognitive behavioral therapy would be important for developing optimal treatment strategies in depression. The SPeED study (Sport/Exercise Therapy and Psychotherapyevaluating treatment Effects in Depressive patients) is a randomized controlled trial to investigate underlying physiological, neurobiological, and psychological mechanisms of the augmentation of cognitive behavioral therapy with endurance exercise. It is investigated if a preceding endurance exercise program will enhance the effect of a subsequent cognitive behavioral therapy. Methods: This study will include 105 patients diagnosed with a mild or moderate depressive episode according to the Diagnostic and Statistical Manual of Mental Disorders (4th ed.). The participants are randomized into one of three groups: a high-intensive or a low-intensive endurance exercise group or a waiting list control group. After the exercise program/waiting period, all patients receive an outpatient cognitive behavioral therapy treatment according to a standardized therapy manual. At four measurement points, major depressive disorder symptoms (Beck Depression Inventory, Hamilton Rating Scale for Depression), (neuro)biological measures (neural activations during working memory, monetary incentive delay task, and emotion regulation, as well as cortisol levels and brain-derived neurotrophic factor), neuropsychological test performance, and questionnaires (psychological needs, self-efficacy, and quality of life) are assessed. Results: In this article, we report the design of the SPeED study and refer to important methodological issues such as including both high- and low-intensity endurance exercise groups to allow the investigation of dose-response effects and physiological components of the therapy effects. Conclusion: The main aims of this research project are to study effects of endurance exercise and cognitive behavioral therapy on depressive symptoms and to investigate underlying physiological and neurobiological mechanisms of these effects. Results may provide important implications for the development of effective treatment strategies in major depressive disorder, specifically concerning the augmentation of cognitive behavioral therapy by endurance exercise.}, language = {en} } @article{KalliesRappFydrichetal.2018, author = {Kallies, Gunnar and Rapp, Michael Armin and Fydrich, Thomas and Fehm, Lydia and Tschorn, Mira and Teran, Christina and Schwefel, Melanie and Pietrek, Anou F. and Henze, Romy and Hellweg, Rainer and Str{\"o}hle, Andreas and Heinzel, Stephan and Heissel, Andreas}, title = {Serum brain-derived neurotrophic factor (BDNF) at rest and after acute aerobic exercise in major depressive disorder}, series = {Psychoneuroendocrinology}, volume = {102}, journal = {Psychoneuroendocrinology}, publisher = {Elsevier}, address = {Oxford}, issn = {0306-4530}, doi = {10.1016/j.psyneuen.2018.12.015}, pages = {212 -- 215}, year = {2018}, abstract = {Physiological mechanisms of an anti-depressive effect of physical exercise in major depressive disorder (MDD) seem to involve alterations in brain-derived neurotrophic factor (BDNF) level. However, previous studies which investigated this effect in a single bout of exercise, did not control for confounding peripheral factors that contribute to BDNF-alterations. Therefore, the underlying cause of exercise-induced BDNF-changes remains unclear. The current study aims to investigate serum BDNF (sBDNF)-changes due to a single-bout of graded aerobic exercise in a group of 30 outpatients with MDD, suggesting a more precise analysis method by taking plasma volume shift and number of platelets into account. Results show that exercise-induced increases in sBDNF remain significant (p<.001) when adjusting for plasma volume shift and controlling for number of platelets. The interaction of sBDNF change and number of platelets was also significant (p=.001) indicating larger sBDNF-increase in participants with smaller number of platelets. Thus, findings of this study suggest an involvement of peripheral as well as additional possibly brain-derived mechanisms explaining exercise-related BDNF release in MDD. For future studies in the field of exercise-related BDNF research, the importance of controlling for peripheral parameters is emphasized.}, language = {en} } @article{TschornRieckmannAroltetal.2019, author = {Tschorn, Mira and Rieckmann, Nina and Arolt, Volker and Beer, Katja and Haverkamp, Wilhelm and Martus, Peter and Waltenberger, Johannes and M{\"u}ller-Nordhorn, Jacqueline and Str{\"o}hle, Andreas}, title = {Erkennungsg{\"u}te dreier deutschsprachiger Screeninginstrumente f{\"u}r Depression bei hospitalisierten Patienten mit koronarer Herzerkrankung}, series = {Psychiatrische Praxis}, volume = {46}, journal = {Psychiatrische Praxis}, number = {1}, publisher = {Thieme}, address = {Stuttgart}, issn = {0303-4259}, doi = {10.1055/s-0042-123434}, pages = {41 -- 48}, year = {2019}, abstract = {Ziel Vergleich der Erkennungsg{\"u}te von drei Depressions-Screeninginstrumenten bei Patienten mit koronarer Herzerkrankung (KHK). Methodik 1019 KHK-Patienten erhielten den Patient Health Questionnaire (PHQ-9 und PHQ-2) und die Hospital Anxiety and Depression Scale (HADS-D) sowie ein klinisches Interview (Composite International Diagnostic Interview) als Referenzstandard. Ergebnisse Bez{\"u}glich der Erkennungsg{\"u}te waren PHQ-9 und HADS-D dem PHQ-2 {\"u}berlegen. Optimale Cut-off-Werte waren 7 (PHQ-9 und HADS-D) und 2 (PHQ-2). Schlussfolgerung PHQ-9 und HADS-D haben eine vergleichbare Diskriminationsf{\"a}higkeit f{\"u}r depressive St{\"o}rungen bei KHK-Patienten.}, language = {de} } @article{KuhlmannTschornAroltetal.2017, author = {Kuhlmann, Stella and Tschorn, Mira and Arolt, Volker and Beer, Katja and Brandt, Julia and Grosse, Laura and Haverkamp, Wilhelm and M{\"u}ller-Nordhorn, Jacqueline and Rieckmann, Nina and Waltenberger, Johannes and Warnke, Katharina and Hellweg, Rainer and Str{\"o}hle, Andreas}, title = {Serum brain-derived neurotrophic factor and stability of depressive symptoms in coronary heart disease patients}, series = {Psychoneuroendocrinology : an international journal ; the official journal of the International Society of Psychoneuroendocrinology}, volume = {77}, journal = {Psychoneuroendocrinology : an international journal ; the official journal of the International Society of Psychoneuroendocrinology}, publisher = {Elsevier Science}, address = {Oxford}, issn = {0306-4530}, doi = {10.1016/j.psyneuen.2016.12.015}, pages = {196 -- 202}, year = {2017}, abstract = {Objective: Brain-derived neurotrophic factor (BDNF) supports neurogenesis, angiogenesis, and promotes the survival of various cell types in the brain and the coronary system. Moreover, BDNF is associated with both coronary heart disease (CHD) and depression. The current study aims to investigate whether serum BDNF levels are associated with the course of depressive symptoms in CHD patients. Methods: At baseline, N = 225 CHD patients were enrolled while hospitalized. Of these, N = 190 (84\%) could be followed up 6 months later. Depressive symptoms were assessed both at baseline and at the 6-months follow-up using the Patient Health Questionnaire (PHQ-9). Serum BDNF concentrations were measured using fluorometric Enzyme-linked immunosorbent assays (ELISA). Results: Logistic regression models showed that lower BDNF levels were associated with persistent depressive symptoms, even after adjustment for age, sex, smoking and potential medical confounders. The incidence of depressive symptoms was not related to lower BDNF levels. However, somatic comorbidity (as measured by the Charlson Comorbidity Index) was significantly associated with the incidence of depressive symptoms. Conclusions: Our findings suggest a role of BDNF in the link between CHD and depressive symptoms. Particularly, low serum BDNF levels could be considered as a valuable biomarker for the persistence of depressive symptoms among depressed CHD patients.}, language = {en} } @article{StroehleBendauAugustinetal.2022, author = {Str{\"o}hle, Andreas and Bendau, Antonia and Augustin, Noah and Esch, Anna Dania and Große, Julia and Kaminski, Jan and Petzold, Moritz Bruno and Plag, Jens and Schmidt, Maike and Sch{\"u}tte, Martina and Strehle, Nicola and Wendt, Nora}, title = {Sportpsychiatrie und -psychotherapie}, series = {Der Nervenarzt : Organ der Deutschen Gesellschaft f{\"u}r Psychiatrie, Psychotherapie und Nervenheilkunde ; Mitteilungsblatt der Deutschen Gesellschaft f{\"u}r Neurologie}, volume = {93}, journal = {Der Nervenarzt : Organ der Deutschen Gesellschaft f{\"u}r Psychiatrie, Psychotherapie und Nervenheilkunde ; Mitteilungsblatt der Deutschen Gesellschaft f{\"u}r Neurologie}, number = {7}, publisher = {Springer}, address = {New York}, organization = {Arbeitsgrp Sportpsychiat Psychothe}, issn = {0028-2804}, doi = {10.1007/s00115-022-01342-x}, pages = {742 -- 753}, year = {2022}, abstract = {Sports psychiatry and psychotherapy is a relatively young field and is comprised of two key segments: the special features of the diagnostics and therapy of mental disorders in elite athletes and the use of exercise and sports in the development and treatment of mental disorders. Although all mental disorders can in principle also occur in (elite) athletes, there are additionally sport-specific mental disorders, such as anorexia athletica and other eating disorders, chronic traumatic encephalopathy, misuse of and dependency on performance-enhancing substances (doping) and muscle dysmorphia. Many high-quality clinical trials over the past two decades have been able to demonstrate a therapeutic efficacy of physical activity and sport in the treatment of various mental disorders. All clinicians active in psychiatry and psychotherapy should possess a basic knowledge of sports psychiatry.}, language = {de} } @misc{TschornKuhlmannRieckmannetal.2020, author = {Tschorn, Mira and Kuhlmann, Stella Linnea and Rieckmann, Nina and Beer, Katja and Grosse, Laura and Arolt, Volker and Waltenberger, Johannes and Haverkamp, Wilhelm and M{\"u}ller-Nordhorn, Jacqueline and Hellweg, Rainer and Str{\"o}hle, Andreas}, title = {Brain-derived neurotrophic factor, depressive symptoms and somatic comorbidity in patients with coronary heart disease}, series = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe}, journal = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe}, number = {1}, issn = {1866-8364}, doi = {10.25932/publishup-55731}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-557315}, pages = {11}, year = {2020}, abstract = {Objective: Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF). Methods: The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment. Results: Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS. Conclusion: Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.}, language = {en} } @article{PetzoldBischoffRogolletal.2017, author = {Petzold, Moritz B. and Bischoff, Sophie and Rogoll, Janina and Plag, Jens and Teran, Christina and Brand, Ralf and Str{\"o}hle, Andreas}, title = {Physical activity in outpatients with mental disorders: status, measurement and social cognitive determinants of health behavior change}, series = {European archives of psychiatry and clinical neuroscience : official organ of the German Society for Biological Psychiatry}, volume = {267}, journal = {European archives of psychiatry and clinical neuroscience : official organ of the German Society for Biological Psychiatry}, publisher = {Springer}, address = {Heidelberg}, issn = {0940-1334}, doi = {10.1007/s00406-017-0772-3}, pages = {639 -- 650}, year = {2017}, abstract = {Physical activity (PA) can play an important role in improving the mental and physical health in patients with mental disorders but is not well studied in this population. The aim of this study was to assess the status of PA in outpatients with mental disorders, compare the convergence of self-rating and accelerometer measurement and examine the influence of social cognitive variables from the Motivation-Volition (MoVo) model and clinical measures on PA. Eighty-four patients were recruited from three psychiatric outpatient clinics and local psychiatrists (Distribution of ICD-10-Diagnoses: F3.x = 59.5\%, F4.x = 20.2\%, F2.x = 17.9\%, F1.x = 2.4\%). PA, Self-efficacy, Outcome-expectancies, Intention, Self-concordance, Action- and Coping-planning, Health-related Quality of Life (SF-12) and Psychiatric Symptoms (SCL-27) were assessed through questionnaires. PA was assessed objectively by accelerometers. Most of the participants did not reach PA recommendations. Subjective and objective measurement of PA showed good accordance for total PA on group level but lower accordance on individual level. Motivational and volitional determinants of health behavior change showed a similar pattern of correlations with PA as in populations without mental disorders. Outpatients with mental disorders have the ability and are willing to perform PA but a large proportion of our sample did not meet PA recommendations. To assess group levels of PA, subjective and objective measurement seem equally apt, for individual diagnostics, a combination of both should be considered. Social cognitive determinants of health behavior change seem to be as helpful for the design of PA interventions for patients with mental disorders as they are in other populations.}, language = {en} } @article{PetzoldMummBischoffetal.2019, author = {Petzold, Moritz Bruno and Mumm, Jennifer Lara Maria and Bischoff, Sophie and Große, Julia and Plag, Jens and Brand, Ralf and Str{\"o}hle, Andreas}, title = {Increasing physical activity and healthy diet in outpatients with mental disorders}, series = {European archives of psychiatry and clinical neuroscience : official organ of the German Society for Biological Psychiatry}, volume = {269}, journal = {European archives of psychiatry and clinical neuroscience : official organ of the German Society for Biological Psychiatry}, number = {5}, publisher = {Springer}, address = {Heidelberg}, issn = {0940-1334}, doi = {10.1007/s00406-018-0941-z}, pages = {529 -- 542}, year = {2019}, abstract = {IntroductionWhile physical activity (PA) can play an important role in the treatment of mental disorders (MD), large proportions of patients with MD do not meet PA recommendations. The aim of this trial was to evaluate whether structured psychological intervention (MoVo-LISA) is effective in helping outpatients with MD to increase their level of PA. As active control group (CG) we modified MoVo-LISA to target healthy diet behavior.MethodsN=83 outpatients with MD (F1-F4) were randomized to the two conditions. PA (self-report and accelerometry), dietary behavior, social-cognitive determinants of health behavior change, psychiatric symptoms and health-related quality of life were assessed at baseline, 1 and 12 weeks after the intervention.ResultsSignificant time*group interaction effects for objectively measured PA, dietary behavior and fruit and vegetable consumption indicated differential effects of the interventions on these outcomes. PA increased in the MoVo-LISA group (IG) from baseline to follow-up while it decreased in CG. IG showed a significant higher level of objectively measured PA at follow-up compared to CG. Dietary behavior and fruit and vegetable consumption significantly increased from baseline to follow-up in CG, but not IG. IG showed a significant increase in some, but not all social cognitive determinants of health behavior change.ConclusionsMoVo-LISA is effective in helping outpatients with MD to increase their level of PA in short- and mid-term. The used intervention strategies are effective for the promotion of healthy diet in patients with MD as well.}, language = {en} } @article{TschornKuhlmannRieckmannetal.2020, author = {Tschorn, Mira and Kuhlmann, Stella Linnea and Rieckmann, Nina and Beer, Katja and Grosse, Laura and Arolt, Volker and Waltenberger, Johannes and Haverkamp, Wilhelm and M{\"u}ller-Nordhorn, Jacqueline and Hellweg, Rainer and Str{\"o}hle, Andreas}, title = {Brain-derived neurotrophic factor, depressive symptoms and somatic comorbidity in patients with coronary heart disease}, series = {Acta Neuropsychiatrica}, volume = {33}, journal = {Acta Neuropsychiatrica}, number = {1}, publisher = {Cambridge Univ. Press}, address = {Cambridge}, issn = {1601-5215}, doi = {10.1017/neu.2020.31}, pages = {22 -- 30}, year = {2020}, abstract = {Objective: Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF). Methods: The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment. Results: Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS. Conclusion: Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.}, language = {en} }