In Germany there is a scientific gap in psychiatry and psychotherapy towards specific aspects of different sexual orientations. There are only a few research studies investigating mental health in gay, lesbian and bisexual people and their special needs in the mental health care system. Non-pathologizing developmental theories and new findings about sexual orientation are hardly recognized in psychiatric textbooks, education and teaching.

Therefore in 2009 the DGPPN Referat “Sexual Orientation in Psychiatry and Psychotherapy” was founded. On the DGPPN congress 2009 the two symposia were organized. In the state of the art symposium specific aspects towards theories and mental health of gay, lesbian and bisexual people were discussed. Also the response of mental health professionals and ethical aspects of interventions aimed at changing sexual orientation were referred. In the second symposium influences of the Third Reich on the psychiatric perspectives towards homosexuality were discussed.

Future goals of the DGPPN Referat are the development of guidelines for treatment, teaching and education in Germany and the establishment of a German and European scientific network.

The presentation highlights the importance of homosexuality in understanding depression and suicidality among men. This issue is not sufficiently acknowledged in research and practice even though international studies report homosexual and bisexual men to be at high risk for depression and suicidality. Results from a meta-analysis of international studies will be presented and they are consonant with the few study results from German speaking countries. In the scientific literature, the increased risk is mostly explained through the harmful effects of “minority stress”, i.e., expected or actual violence and discrimination resulting from being homosexual or bisexual. In addition to minority stress, many homosexual and bisexual men are also confronted with negative social reactions long before coming out because of gender role nonconformity, and that increases the risk for later psychological distress. These findings highlight the need to consider sexual orientation issues in the prevention and treatment of depression and suicidality. There has been some progress in this respect but examples of related ignorance are encountered in the current mental health literature and in suicide prevention programs.

SAYLE is a health promoting programme, funded by the EU Commission for adolescents in European schools. Its main objectives are to lead adolescents to better health through decreased risk taking and suicidal behaviours, to evaluate outcomes of different preventive programmes and to recommend effective culturally adjusted models for promoting health of adolescents in different European countries. It is developed by a consortium of 12 countries: Austria; Estonia; France; Germany; Ireland; Hungary; Italy; Israel; Romania; Slovenia; Spain and Sweden (coordinating centre). In this health promotion programme, an intervention study will be implemented to assess the effects of three different health promoting/suicide preventing programmes in comparison with control groups in 11,000 students across 12 European countries. The three interventions are:

1. 1. A general health promotion programme targeting students awareness on healthy/unhealthy behaviors and students self-efficacy in diminishing unhealthy behaviors;

2. 2. TeenScreen - screening by professionals of at-risk students through a questionnaire. For adolescents identified as high risk, the program includes individual assessment and referral to mental health treatment and measures ensuring compliance;

3. 3. QPR (Question, Persuade & Refer) - a gatekeeper's program, training all adult staff at schools (teachers, counselors, nurses etc) and parents on how to recognize and refer a student with risk-taking behaviours or those suffering from mental illness to mental-health help resources.

Catatonia is an intriguing psychopathological dimension and the discussion about the clinical relevance of catatonic symptoms in psychiatry is continuing for at least 125 years. The debate started from the original description by Kahlbaum and was further elaborated by Kraepelin and Bleuler who incorporated catatonia in their broad concept of schizophrenia. They regarded catatonic symptoms merely as an integral part of schizophrenia. In addition, periodic catatonia was described by Leonhard that has a considerable hereditary loading, shows a phasic course with alternating hyperkinesia and akinesia and can be delineated from the akinetic-hyperkinetic motility psychosis which belongs to the cycloid psychoses.

Over the past decades, the prevalence of the diagnosis of catatonia as a separate disease and as subtype of schizophrenia is decreased considerable. This phenomenon is most probably the result of changes in the diagnostic criteria as well as underrecognition of this symptom dimension.

Today's research is focussing on the pathophysiology, genetics and treatment of catatonia. As demonstrated in factor analytical studies, this disorder can be considered as a separate psychopathological dimension. Apart from the endogenous catatonias belonging to either the periodic catatonia or catatonic schizophrenia, the catatonic dimension is present in about ten percent of newly admitted patients with affective or schizophrenic psychoses.

In for different presentations, the need for a differential diagnosis of catatonias will be outlined as well as their genetic and pathophysiological backgrounds and appropriate treatment strategies, such as electroconvulsive therapy.

Originally considered by Kahlbaum to be an independent disease entity characterized by mental and motor abnormalities, catatonia was later viewed as a subtype of schizophrenia as it is the case in current classifications like ICD-10 and DSM-IV. Since catatonic symptoms were observable not only in schizophrenic psychoses, but also in affective, somatic or even psychogenic disorders, many researchers today consider catatonia as a nosologically unspecific syndrome. In the end, the traditional conceptions did not succeed in defining catatonia as a clinically homogeneous and valid diagnosis.

An independent conception of catatonia was elaborated by the Wernicke-Kleist-Leonhard school of psychiatry. Based on a precise differentiation of diagnostically specific qualitative psychomotor disturbances, two essentially distinct forms of catatonic psychoses have been separated which differ in symptomatology, prognosis and treatment: on the one hand periodic catatonia, and on the other hand the group of systematic catatonias.

Periodic catatonia usually has an acute onset, shows a bipolar and polymorphous symptomatology and runs an intermittent course. After one or more acute attacks, adynamic residual states of varying degrees of severity develop. Hyperkinetic and akinetic distortions of psychomotor activity are characteristically intermingled in attacks and residual states.

In contrast, systematic catatonias begin insidiously, run a chronically progredient course without remissions and develop clear-cut and stable residual states. Six subtypes can be distinguished, each of which is characterized by a specific symptom constellation.

Catatonia has attracted increasing attention in relation to basic theoretical problems of psychiatry. Periodic catatonia (MIM 605419) is characterized by qualitative hyperkinetic and akinetic psychomotor disturbances through psychotic episodes, and debilitating symptoms in the long term with psychomotor weakness, grimacing facial movements, and apathy. Our aim was to identify new association loci for periodic catatonia a subphenotype of schizophrenic psychoses. We therefore performed a genome-wide association analysis using SNP Microarray and DNA pooling (SNP-MaP) with 500K Affymetrix arrays. We pooled DNA of 245 cases in three biological replicates (n=84, 84, 77) and 216 controls in two biological replicates (n=108, 108). All pools were processed in three technical replicates. Array data was analysed with a modified version of GenePool. We determined the mean relative allele signal value (RAS) of the technical replicates of each pool and compared each case pool with the combined controls. We used a 5-SNP sliding window approach and defined clusters as potentially associated loci if they overlapped in all biological replicates. We then verified pooling data at single genotype level for associated array SNPs at five selected loci using TaqMan assays in an extended cohort (344 cases, 585 controls). Two of these loci showed significant association at single marker (p=0.0002) and haplotype levels (p=0.0042), even after permutation correction (pc=0.0007; pc=0.0224). Our data show that hybridization intensities of pooled DNA correlate well with individual genotyping results. Thus DNA pooling is a useful strategy for GWAS since we were able to detect significant association loci in a complex disease.

The history of electrophysiological methods in Psychiatry is studded with ups and downs. Recently, several factors contributed to the renascence of the electrophysiological methods in schizophrenia research; in particular: a) the validation of previously reported electrophysiological findings by means of functional brain imaging techniques; b) the possibility offered by electrophysiological techniques to study brain's systems physiological and pathological activity with a high temporal resolution; c) a different conceptualizations of psychopathological phenomena, no longer considered as the result of a dysfunction of one or more brain regions, but as a consequence of the failure to integrate the activity of different areas. Main deliveries of such renascence include: advances in the study of abnormal functional connectivity underlying schizophrenia symptoms and the identification of electrophysiological endophenotypes. Notwithstanding the fact that electrophysiological abnormalities were shown to be related to diagnostic subtypes, risk factors, symptom dimensions and prognosis, electrophysiological methods are still of limited impact in clinical settings, and their application is confined to the exclusion of “organic” brain pathology.

Depression is a frequent co-morbid condition in diabetic patients. In controlled studies 9% fulfilled criteria for major depression and 26% reported elevated depressive symptoms. Depression rates are twofold higher in diabetic patients than in the non-diabetic population (major depression 5%; elevated depressive symptoms 14%). Diabetes specific risk factors like occurrence of complications, poor glycaemic control, insulin therapy in type 2 diabetic patients are statically associated with elevated depression rates. Furthermore the presence of depressive symptoms in non-diabetic subjects is associated with a significant higher diabetes risk in the future.

Depression in diabetic patients is linked with poorer diabetes self care behaviour like adherence to medication, keeping a healthy diet and physical exercise. The co-morbidity of diabetes and depression has also a negative impact on quality of life, which is greater than the comorbidty of depression and other chronic somatic diseases. Longitudinal studies indicate that depression in diabetes is related to a poorer prognosis. The risk for the development of complications is significantly higher in depressed than in non-depressed diabetic patients. Representative studies showed a significantly higher mortality in diabetic patients with depression than in non-depressed diabetic patients (hazard ratios between 1.67 to 2.6). The results also suggest that these negative consequences of depression are not only present in diabetic patients with severe forms of depression but also in patients with rather mild depression. In summary epidemiological findings imply that depression in diabetes is an important clinical condition warranting clinical attention as well as scientific interest.

The mechanism or pathogenesis that underlies the strong association between depression and diabetes is poorly understood but there are tentative models to explain the co-morbidity. The conventional model, namely that the psychological burden of living with diabetes leads to higher rates of depression, is not fully supported by the current evidence. Additional models include

1. a) the possibility of shared developmental origins between diabetes and depression

2. b) the direct effects of hyperglycaemia, hypoglycaemia and related metabolic dysfunction on the brain and

3. c) common mediators such as chronic stress response leading to pro-inflammation.

The potential for research into the above postulated pathways is vast and may lead to identification of new modifiable targets for intervention.

In this lecture, an overview will be given of the literature concerning treatment for comorbid diabetes and depression. A systematic review and analysis will be presented. It turns out that, although many clinicians and researchers find this an important subject of research, and although the clinical implications of such research seem obvious, randomized clinical trials evaluating effectiveness of treatment are scarce and often the numbers of patients included are small. However, all RCTs point in the direction of efficacy of treatment of this combined condition in terms of combined impact. Severity of depressive symptoms and glycemic control are most often used as outcome measures. Psychotherapeutic interventions show a moderate to large effect on both ; antidepressant treatment as well as collaborative care show moderate effects on depressive symptom severity. The clinical, public health and research implications of these findings will be discussed.

Diabetes and depression on their own are debilitating and costly diseases. Their co-existance presents further treatment and funding challenges. This session will provide an overview of the economic dimensions of this comorbid relationship and present the findings of a systematic review of evidence related to this. The review found a growing literature demonstrating: increased resource use and health care costs, unemployment and lost productivity; poorer quality of life; and a higher risk of mortality arising from the co-existance of these illnesses. While there are some good quality studies evaluating the efficacy/effectiveness of various treatments, few include an economic evaluation and the generalisability of those is unclear. Therefore, while the evidence suggests little doubt of the broad-ranging economic impacts on patients, health care systems and wider society, there is still a gap regarding the cost-effectiveness of alternative approaches to the treatment and long-term management of this comorbidity within the context of limited health care budgets.

Subclinical depression is a condition in which a person has clinically relevant depressive symptoms, but does not meet criteria for a depressive disorder. In this presentation, the different operationalizations of subthreshold depression will be presented, and we will focus on the importance from a clinical point of view, as well as from a public health public point of view. Subthreshold depression has important consequences for the quality of life, but not as much as major depression. It also results in huge economic costs on the individual level, but again less than the costs associated with major depression. Because subthreshold depression is more prevalent, the total costs of subthreshold depression on the population level are, however, comparable to those of major depression. It is also clear that subjects with subthreshold depression have an increased risk of developing a major depression. How large that chance is depends on several factors, including the definition of subthreshold depression. Finally, the results of a meta-analysis will be presented in which the effects of psychological treatments of subthreshold depression are examined. This meta-analysis shows that psychological treatments can be treated effectively, and there is a trend indicating that these interventions can prevent the onset of major depression.