ADHD is frequently diagnosed in children and adults. The disorder is highly heritable. However, the genetic architecture of ADHD is complex, with multiple genetic variants of individually small effect size contributing to disease in most patients.

In our own studies as well as in the large mega-analyses of the ENIGMA ADHD Working Group, we have investigated the brain substrates of ADHD. We find the disorder to be characterized by delayed sub–cortical and cortical growth of gray matter in childhood, which gradually normalizes in adulthood: sub–cortical volumes as well as cortical thickness and surface area are smaller in children with ADHD, but become indistinguishable from healthy individuals in adulthood. The situation looks different for white matter connectivity: both in childhood and adulthood, widespread differences in the major white matter tracts are found. The pattern of findings suggests that alterations in myelination might lie at the basis of such case-control differences. Since the disorder and many brain structural measures affected in ADHD are highly heritable, we investigated the overlap of genetic risk factors for ADHD with genetic factors involved in brain volume. This resulted in the identification of several genetic variants contributing to disease risk as well as ADHD-related brain phenotype.

In conclusion, we find ADHD to be a disorder of delayed brain maturation in terms of gray matter, but of persistently altered white matter connectivity across the lifespan. Genetic factors influencing both disease risk and brain measures might improve our understanding of disease etiology and persistence.

Previous MRI studies of bipolar disorder (BD) are often limited by small sample sizes and heterogeneity exists with regard to neuroimaging markers. To address these limitations, the ENIGMA Bipolar Disorder Working Group collected the largest BD neuroimaging data set ever studied (n = 6,500). Here, we review findings from sub–cortical volume and cortical thickness and area analyses.

ENIGMA harmonized analysis methods were applied to 28 international pooled study samples of MRI data and involved sub–cortical and cortical imaging analyses. We assessed differences between BD and healthy controls (HC) using both mega and meta–analytic multiple linear regression models, adjusting for standard covariates (age, sex, etc.), and correcting for multiple comparisons.

Sub–cortical volume analysis revealed we found consistent volumetric reductions in BD patients for hippocampus and thalamus and enlarged lateral ventricles in patients. In BD, cortical gray matter was thinner in frontal, temporal and parietal regions of both brain hemispheres. BD had large general effects on mean gray matter thickness in both left and right brain hemispheres. Further we found that psychopharmacological treatment showed significant associations with cortical thickness and surface area.

The ENIGMA pipeline allows for identification of brain MRI abnormalities in BD in the largest analysis ever conducted. The results suggest a pattern of brain structure abnormalities, which provide novel insight in pathophysiology of BD, and potential effects of mood stabilizing agents.

Over the last decades, in matters of the assessment of psychopathology and its clinical consequences, there has been an increased interest in neurocognitive function including non-social and social cognition.

Classic psychopathology -as represented e.g. by the standardized AMDP system- focuses on pathognomonic signs for the categorization of syndromes [1] and differentiates between disturbances of perception, concentration, memory retention and long-term memory. A recent short screen for cognitive impairment in psychiatry (SCIP) has addressed five domains of cognitive function: verbal learning–immediate, working memory, verbal fluency, verbal learning–delayed and processing speed [2].

Using the SCIP in admissions from a defined catchment area in the southwest of Vienna we confirm the presence of cognitive deficits in schizophrenic patients and to a lesser degree in bipolar patients. The deficits were present in all five domains and no discriminatory pathognomonic signs could be found between schizophrenia and bipolar disorder.

Recently, possibly selective deficits in social cognition have been described in schizophrenic patients [3]. We review the evidence on the specificity of social impairment to schizophrenia.

As in all medical disciplines, diagnosis in clinical psychiatry should be reached in a step-wise approach: after assessing the chief complaint of the patient, a careful examination of the psychopathology follows e.g. by using the AMDP system [1] to preliminarily conclude the process with a syndromal classification [2]. This syndromal classification is of great importance as it guides the initiation of therapy in daily life practice. After gaining additional information (e.g. investigation in the course of the disease, brain imaging, thorough assessment of cognitive function, exclusion of organic causes) a final diagnosis is possible. Unfortunately, a premature jumping to diagnosis is not uncommon (with the potential consequence of incorrect therapies).

In addition to these difficulties, recent neurobiological research has shown that nosologic assignments through conventional diagnostic classifications are far less specific than assumed, revealing a large overlap between diagnostic categories [3,4], e.g. between Schizophrenia and affective disorders. Consequences of this finding are discussed both for the construction of future classification systems and for therapy.

Autism spectrum disorders (ASD) and schizophrenia were separated into different diagnostic categories in the late 1970's (DSM-III) having previously been considered as related diagnostic entities. Since then, several lines of evidence have indicated that these disorders show clinical and cognitive overlaps as well as some common neurobiological characteristics. Furthermore, there is a group of patients presenting with ASD and psychotic experiences who pose particular diagnostic and management challenges and may represent a subgroup of ASD more closely linked to psychosis. Evidence from a study of the first empirically derived classification of children with ASD in relation to psychosis based on three underlying symptom dimensions, anxiety, social deficits and thought disorder, will be presented. Further phenomenological, genetic and neuroimaging research on the clinical boundaries and overlapping pathophysiology of ASD and psychosis may help better define their relationship and lead to more effective interventions. Understanding this relationship will also provide a framework of working with patients with mixed clinical presentations.

Autism Spectrum Disorders (ASD) is a group of neurodevelopmental disorders with heterogeneous etiology characterized by deficits in social cognition, communication, and behavioral flexibility. Disturbances on molecular and cellular level in early brain development incl. intercellular communication, an unbalanced ratio between certain neuronal populations and maturation/differentiation process, oxidative stress, happening in embryonal stages, might be promising candidates to explain the development of autistic symptoms.

In order to get a deeper understanding of these processes, valid “disease models” are pivotal. A new cutting edge technique, named brain organoids, has been highlighted as a promising candidate for obtaining a better “disease model”.

Brain organoids derived from patients induced pluripotent stem cells (iPSC) follow in vivo timeline development; they also have the ability to recreate the right complexity of the brains, developmental stages. On the cellular and gene expression level, organoids demonstrate a high similarity to the developing brain in vivo and can therefore recapitulate early stages of the neurogenesis. To date organoids are the most relevant cellular in vitro platform for the understanding of the mechanisms behind ADS pathology. Investigations of “mini brains” at different time points in their development will give a wider and more detailed picture of the disease dynamic and thus the development of therapeutic and prevention strategies. It is a tool that can be used for effective high throughput screening of chemical compounds as potential drugs (“in sphero” drug testing). Organoids are a good modeling system for elucidating the role of epigenetic and environmental factors for development of ASD.

Structural and functional brain alterations as well as cognitive deficits are well-documented findings in schizophrenia patients. Cognitive impairments affect the long-term outcome of schizophrenia and are the main contributors to disability. Despite their clinical impact, however, no effective options are available to treat them sufficiently. Aerobic endurance training has been shown to have effects on brain plasticity, gray and white matter volume as well as functional connectivity measures and on cognitive functioning in animal models and healthy humans. However, effects of physical exercise in combination in combination with cognitive remediation are unknown in Schizophrenia. 21 chronic schizophrenia patients and 21 age and gender–matched healthy controls underwent 3 months of aerobic exercise (endurance training, 30 min, 3 times per week). 21 additionally recruited schizophrenia patients played table soccer (known as “foosball” in the USA) over the same period. After 6 weeks of endurance training or table soccer, all participants commenced standardized cognitive training with a computer-assisted training program. We could show that a 3-month endurance-training program combined with CR therapy had positive effects on everyday functioning in multi-episode Schizophrenia patients. Deficits improved from medium to mild as assessed with the GAF. Negative symptoms, short and long-term verbal memory and cognitive flexibility also improved with training. We could demonstrate grey matter volume increase in the left temporal lobe in schizophrenia patients undergoing endurance training. A non-endurance and coordinative training stimulus like playing table soccer led to a clearly distinct pattern of grey matter alterations in Schizophrenia patients.

Cognitive Remediation Therapy (CRT) deals with the cognitive impairment, which is one of the most disabling symptoms of schizophrenia. Unfortunately, the understanding of its neurobiological correlates is far from complete. Neuroimaging studies have shown that CRT is able to induce neurobiological changes although the results have not always been enough replicated. The most commonly reported changes were those that involved the prefrontal and thalamic regions. Additionally, structural changes were described in both the grey and white matter, suggesting a neuroprotective effect of cognitive remediation. Neuroimaging studies of cognitive remediation in patients with schizophrenia suggest a positive effect on brain functioning in terms of the functional reorganisation of neural networks. From a different perspective, some changes in serum levels of Brain derived neurotrophic factor (BDNF) have been described. However, our replication of this trial has not been able to find any significant differences. So, nowadays the status of BDNF as a biomarker of cognitive recovery is possibly premature. One possible explanation can be the role of genetics and their different polymorphisms. COMT and BDNF polymorphisms could be accounting for the different outcomes of CRT. Moreover, some studies suggested a role of genes affecting dopamine modulation on outcomes of cognitive remediation.

Cognitive remediation (CR) has proved to be effective in improving cognition, symptoms and psychosocial functioning in schizophrenia and other psychoses, but its impact on the use of psychiatric services and patterns of care of patients suffering from these diseases is still scarcely known. In fact, it would be particularly relevant to know if such intervention may have any modifying effect on use of services and costs of treatments. There is preliminary evidence that such an impact does exist, with possible reduction of number and duration of hospitalizations and of long-term residential stays and consequent reduced costs of inpatient treatment. On the other hand, community treatment costs could be increased as an effect of a shift of psychiatric and psychosocial interventions from inpatient to outpatient activities. A critical review of the existing literature on the issue will be provided, together with a discussion of the impact of this shift towards the attainment of increased functional and social recovery in the individual patient.

Electrodermal Activity (EDA) refers to changes in electrical conductance of the skin. Electrodermal hyporeactive individuals are those who show an unusual rapid habituation to identical non-significant stimuli. Previous findings suggested that electrodermal hyporeactivity has a high sensitivity and a high negative predictive value for suicide. The aim of the present study is to test the effectiveness and the usefulness of the EDOR® (ElectroDermal Orienting Reactivity) Test as a support in the suicide risk assessment of depressed patients.

One thousand five hundred and seventy three patients with a primary diagnosis of depression, whether currently depressed or in remission, have been recruited at 15 centres in 9 different European countries. Depressive symptomatology was evaluated through the Montgomery-Asberg Depression Scale. Previous suicide attempts were registered and the suicide intent of the worst attempt was rated according to the first eight items of the Beck Suicide Intent Scale. The suicide risk was also assessed. During the EDOR® Test two fingers are put on gold electrodes and a moderately strong tone is presented through headphones now and then during the test. The EDOR® Test is able to register the electrodermal responses to those tones, along with the blood volume in the fingers. Each patient is followed up for one year in order to assess the occurrence of suicidal behaviors.

Expected results would be that patients realizing a suicide attempt with a strong intent or committing suicide should be electrodermally hyporeactive in most cases and non-hyporeactive patients should show only few indications of death intent or suicides. Preliminary findings will be presented.

Suicidal behavior and its prevention constitute a major public health issue, and the moderating effect of sociodemographic factors has been studied for more than a century. In the last years it has become evident that the relationship between social factors and suicidal behavior is complex and highly dependent on the context. For instance, minorities suffering marginalization, such as the Inuit in Canada or the aborigines in Australia, present high rates of suicide. However, other minorities, such as immigrants arriving to tightened communities, can be protected from suicide compared to the social majority. Other contradictory effects have been reported concerning income per capita and the evolution of the economy. Unfortunately, the interplay of social factors in suicidal behavior and the social consequences of suicide attempts are rarely represented in theoretical models of suicidal behavior, despite their importance to adapt suicide prevention policies to social groups at risk. In this presentation, recent advances and new and integrative avenues for future research in the social aspects of suicidal behavior will be summarized.

Psychiatric illness, psychotropic drugs and driving ability. For most people driving is an important activity in daily life affecting physical, social, and economic well-being. Driving mobility is also an important part of one's self-identity that may influence health status. It could be demonstrated that 67% of psychiatric patients reported to have a valid driver's license and 77% of them referred to regularly use their cars. Closer inspection of data reveals, that road mobility is largely linked to psycho-functional status. In this context a significant issue is the impact of medical conditions and/or psychoactive medicines on road safety. Psychiatric patients, considered as a group, seem to have a moderately elevated risk of being involved in a road traffic accident with high-risk rates especially for organic mental disorders. With respect to pharmacotherapy, within psychotropic medicines an increased road traffic crash risk for benzodiazepines, z-hypnotics and some antidepressants has been well documented. The combination of psychoactive drugs additionally increases risk that is highest when combined with alcohol. However, therapeutic drug use may also lower risk, as the illness itself constitutes a higher risk of road traffic accidents. As many studies did not adequately control for confounding factors, results of epidemiological studies must be interpreted cautiously.

Driving a vehicle is an important everyday life skill associated to a psychiatric patient's autonomy and identity. Nevertheless, the right to drive is not a right at all, it is a privilege granted and regulated by rules and restrictions from the States that have also the duty to pull this privilege and deny the ability to legally drive in potentially unsafe drivers. The decision about for whom and when to forbid driving is a difficult matter of judgment that must remain a clinical and professional judgment within the medical encounter. Both antipsychotics as the psychiatric disorders target of these psychoactive drugs produce changes of psychomotor performance that can interfere with the ability to drive safely. Moreover, it is really hard to distinguish between the effects of the disease itself as opposed to the effects of the medication when studying the interaction between antipsychotics and driving ability. Previous results of our research in the field indicate that psychiatric patients who improved clinically after drug treatment also showed improvements in driving ability. So, adequate psychotropic treatment causes a positive effect on driving performance that outweighs the possible deleterious effect of medication. However, it remains essential to supply mental health professionals with new information, which is quantitatively and qualitatively valid, on the role of antipsychotics in driving ability. The purpose of the present lecture is to review research undertaken to-date on the effects of antipsychotic medications on driving ability. A search of various databases, including Medline, Embase and PsycInfo, will be conducted.