Video is considered to be an effective, easy to use tool employed in anti-stigma interventions among young people. Mass media has been shown to be effective for reducing stigma; however, there is insufficient evidence to determine the destigmatization effects of videos specifically. This article systematically reviews the effectiveness of video intervention in reducing stigma among young people between 13 and 25 years. We searched 13 electronic databases including randomized controlled trials, cluster randomized controlled trials, and controlled before and after studies. Of the 1426 abstracts identified, 23 studies (reported in 22 papers) met the inclusion criteria. Video interventions led to improvements in stigmatising attitudes. Video was found to be more effective than other interventions, such as classical face-to-face educational sessions or simulation of hallucinations. According to results of two studies, social contact delivered via video achieved similar destigmatization effect to that delivered via a live intervention. Although the quality of studies as well as the form of video interventions varied, the findings suggest that video is a promising destigmatization tool among young people; however, more studies in this area are needed. There was a lack of evidence for interventions outside of school environments, in low- and middle-income countries, and studies, which looked at long-term outcomes or measured impact on actual behaviour and implicit attitudes. The review generates recommendations for video interventions targeted at young people.

When directly perturbed in healthy subjects, premotor cortical areas generate electrical oscillations in the beta range (20–40 Hz). In schizophrenia, major depressive disorder and bipolar disorder (BD), these oscillations are markedly reduced, in terms of amplitude and frequency. However, it still remains unclear whether these abnormalities can be modulated over time, or if they can be still observed after treatment. Here, we employed transcranial magnetic stimulation (TMS) combined with EEG to assess the frontal oscillatory activity in eighteen BD patients before/after antidepressant treatments (sleep deprivation and light therapy), relative to nine healthy controls. In order to detect dominant frequencies, event related spectral perturbations (ERSP) were computed for each TMS/EEG session in all participants, using wavelet decomposition. The natural frequency at which the cortical circuit oscillates was calculated as the frequency value with the largest power across 300 ms post-stimulus time interval. Severity of depression markedly decreased after treatment with 12 patients achieving response and nine patients achieving remission. TMS/EEG resulted in a significant activation of the beta/gamma band response (21–50 Hz) in healthy controls. In patients, the main frequencies of premotor EEG responses to TMS did not significantly change before/after treatment and were always significantly lower than those of controls (11–27 Hz) and comparable in patients achieving remission and in those not responding to treatment. These results suggest that the reduction of natural frequencies is a trait marker of BD, independent from the clinical status of the patients. The present findings shed light on the neurobiological underpinning of severe psychiatric disorders and demonstrate that TMS/EEG represents a unique tool to develop biomarkers in psychiatry.

In the past few years, it has become a sort of cliché to state that psychiatry is in a crisis. In particular, it has been repeatedly argued that: (a) psychiatric diagnoses are invalid; (b) psychiatric research has not progressed significantly (in particular, it has not been able to identify “the cause” of schizophrenia, depression or bipolar disorder); (c) psychiatric treatments are of limited value, and their widespread use has not been able to reduce the incidence of mental disorders. This perception of crisis has been at least in part generated by an identification of mainstream psychiatry with the neo-kraepelinian paradigm, so that the crisis of confidence in that paradigm has expanded into a crisis of confidence in the psychiatric discipline. According to Kuhn, the crisis of confidence in a paradigm is accompanied by a period of “extraordinary science”, marked by a proliferation of competing methodologies, the proposition of a variety of divergent solutions for the problem defining the crisis, and the recourse to philosophy and to debate over fundamentals of the discipline. The crisis of confidence in the neo-kraepelinian paradigm has generated such a period, in which we are all now immersed. In this presentation, I will summarize the main components of the neo-kraepelinian paradigm; I will illustrate why that paradigm has failed, or at least has lost people's confidence; and will summarize the main elements which are emerging in the current period of “extraordinary science”.

Public mental health and clinical psychiatry: Are they two separate worlds?

Stefan Priebe, unit for social and community psychiatry, Queen Mary University of London.

Public mental health focuses on health indicators and interventions on population level with an emphasis – although not exclusively–on prevention. In contrast, clinical psychiatry involves treatment of individuals in the setting of a health service and deals with people who usually already have a mental disorder. The theoretical background, the underpinning evidence and the practical approach of public mental health and clinical psychiatry differ from each other and concepts of one of the two cannot easily be transferred to the other.

Nevertheless, the presentation will argue that there are also links between the two. These links may be based on overall applicable values, a common understanding of mental disorders, and social models of overcoming mental distress. These links can have implications for how clinical psychiatrists are engaged in political and societal activities, get involved with local communities, and work in daily practice with their patients.

The public mental health perspective, used in a wide sense of the term, has played a substantial role in the historical development of psychiatry, including its major reforms, and might also open up how clinical psychiatry might be attractive as a career option and relevant as a profession in the future.

The concept of schizophrenia has undergone many changes since its first inception in the early 20th century. Basically, the concept has stood the tests of time, as it provides useful information about the clinical picture, the clinical course and the available treatment modalities. Any alternative concept will need to show that it provides similar information. The concept has also been useful to establish evidence–based guidelines for diagnosis and treatment, and to provide valuable information as regards psychosocial outcomes. In addition, recent genetic and neurophysiological studies have shown that common grounds of aetiopathogenesis can be identified, in that schizophrenia is a mental disorder with some genetic influences and a common pathway in complex disturbances of brain circuits due to altered neurotranmission. Current research focuses on identifying biomarkers for early detection, another area of mental healthcare in which a staging model of schizophrenia proved useful. This presentation will highlight the most pertinent arguments for keeping schizophrenia as a useful diagnostic and therapeutic concept of a mental disorder.

The analysis of the historical development of the currently used diagnosis schizophrenia in DSM or ICD classification indicates that sticking to established terms and methodologies more and more develops to an obstacle in schizophrenia research. The aim of the currently used operational diagnostic approach was to reach reliability of diagnoses between different psychiatrists and researchers as high as possible. This should improve the communication between different research groups and better the comparison of study results. The aim of a high reliability has surely been reached, however, the expected striking progress in research and clinical praxis failed to materialize till today. Reliability, which means agreement, does not simultaneously means validity. Modern brain and genetic research requires more homogenous clinical syndromes or ‘diseases’ to examine them with scientifically based methodologies and technologies. The prerequisite for doing this, however, is going back to clinical and empirical realities and to integrate these realities into the development of a new generation of classification systems that are free of dogmatic thinking.

Major depressive disorder (MDD) is a severe psychiatric syndrome with very high prevalence and socioeconomic impact. Monoamine-based antidepressant drugs (AD) display slow onset of action and limited efficacy. Preclinical studies show that ADs trigger a series of slow adaptive mechanisms that limit the clinical response. These mechanisms result from the pharmacological blockade of monoamine transporters (SERT, NET) and involve presynaptic, such as autoreceptor desensitization (e.g., 5-HT1A and 5-HT1B for serotonin neurons) as well as postsynaptic mechanisms, such as increased neurogenesis and expression of trophic factors, increased dendritic complexity, etc.

Given the strong homeostasis of serotonin and noradrenaline neurons, a way to improve antidepressant action is to prevent self-inhibitory presynaptic mechanisms mediated by auto- and heteroreceptors after reuptake blockade. This strategy was used in the past with the non-selective 5-HT1A antagonist pindolol and has been incorporated by two recently developed AD (vilazodone and vortioxetine). Likewise, new molecular strategies using RNA interference (RNAi) show that the modulation of gene expression in serotonin neurons offers a great potential. Hence, local or intrnasal administration of small interfering RNA (siRNA) molecules targeting SERT or 5-HT1A autoreceptors evokes rapid and robust antidepressant-like effects in rodents.

Moreover, glutamatergic drugs such as the non-competitive NMDA receptor antagonist ketmaine, offer a potential for the development of fast-acting AD due to its rapid and persistent antidepressant effects in treatment-resistant unipolar and bipolar patients after single i.v. infusion, an effect that likely involves the activation of AMPA receptors in ventral areas of the cingulate gyrus and the subsequent fast activation of serotonergic function.

Patients with schizophrenia exhibit a reduced life expectancy. Although unhealthy lifestyle or suicide risk plays a role, the main causes are diverse medical conditions such as cardiovascular diseases, type 2 diabetes mellitus and metabolic syndrome. Albeit pharmacological secondary side effects might also trigger previous conditions, studies in naïve patients reflect diverse anomalies at the onset. Patients with a first episode of psychosis, display a wide scope of metabolic abnormalities, ranging from normality till pathological values depending on the parameters studied. We attempted to evaluate the metabolic syndrome and glycemic homeostasis in a subset of antipsychotic-naïve patients with a first episode of non-affective psychosis. Patients (n = 84) showed a similar prevalence of metabolic syndrome compared with a matched control sample (n = 98) (6% vs 4%, P = 0.562), while glucose homeostasis values differed significantly (14% vs. 5%, P = 0.034). Our results suggest that metabolic syndrome is not a useful clinical condition to be evaluated in patients before pharmacological treatment. Abnormal glycemic homeostasis at the onset of the disease requires specific diagnostic tools and preventive measures in order to avoid future cardiovascular events. New strategies must be implemented in order to evaluate the cardiovascular risk and subsequent morbidity in patients at the onset of the disease.

Response to antidepressants in major depressive disorder is highly variable and determinants are not well understood. Presentation will provide clinical trial data on time to response and determinants of response to antidepressant treatment. Data is from the Innovative Medicines Initiative funded NEWMEDS collaboration, a large public-private collaboration which assembled the largest dataset of individual patient level information from randomized placebo-controlled trials of antidepressant drugs. Studies were conducted by four large pharmaceutical companies. Dataset includes placebo-controlled trials of citalopram, duloxetine, escitalopram, quetiapine and sertraline in adults with MDD. We examined patient and trial-design-related determinants of outcome as measured by change on Hamilton Depression Scale or Montgomery–Asberg Depression Rating Scale in 34 placebo-controlled trials (drug, n = 8260; placebo, n = 3957). While it is conventional for trials to be 6–8 weeks long, data presented will show that drug-placebo differences were observable at week 4 with nearly the same sensitivity and lower dropout rates. Having any of these attributes was significantly associated with greater drug vs. placebo differences on symptom improvement: female, patients being middle aged, increasing proportion of patients on placebo, excluding all patients from centers with high placebo response regardless of active treatment response, using active run in periods and including self-report measures. Proof of concept trials can be shorter and efficiency improved by selecting enriched populations based on clinical and demographic variables, ensuring adequate balance of placebo patients, and carefully selecting and monitoring centers. In addition to improving drug discovery, patient exposure to placebo and experimental treatments can be reduced.

There are large treatment gaps in relation to schizophrenia across all European countries, either because the illness is not recognised or because the response from treatment and care services is inadequate - not evidence-based. This could be because of resource or other constraints. The consequence can be very damaging indeed for individuals with schizophrenia, their families and for the wider society. In this talk I will set out the economic consequences of not identifying or responding appropriately to schizophrenia. Evidence will be drawn from a number of studies, but will be channelled to show new findings in relation to both England and Czech Republic. These figures add to the argument for earlier and better treatment, to benefit everybody including public and private budgets.

Catechol-O-methyltransferase (COMT) inactivates catecholamines, Val/Val genotype was associated to an increased amygdala (Amy) response to negative stimuli and can influence the symptoms severity and the outcome of bipolar disorder, probably mediated by the COMT polymorphism (rs4680) interaction between cortical and subcortical dopaminergic neurotransmission. The aim of this study is to explore how rs4680 and implicit emotional processing of negative emotional stimuli could interact in affecting the Amy connectivity in bipolar depression. Forty-five BD patients (34 Met carriers vs. 11 Val/Val) underwent fMRI scanning during implicit processing of fearful and angry faces. We explore the effect of rs4680 on the strength of functional connectivity from the amygdalae to whole brain. Val/Val and Met carriers significantly differed for the connectivity between Amy and dorsolateral prefrontal cortex (DLPFC) and supramarginal gyrus. Val/Val patients showed a significant positive connectivity for all of these areas, where Met carriers presented a significant negative one for the connection between DLPFC and Amy. Our findings reveal a COMT genotype-dependent difference in corticolimbic connectivity during affective regulation, possibly identifying a neurobiological underpinning of clinical and prognostic outcome of BD. Specifically, a worse antidepressant recovery and clinical outcome previously detected in Val/Val patients could be associated to a specific increased sensitivity to negative emotional stimuli.

Early Intervention services with team-based intensive case management and family involvement are superior to standard treatment in reducing psychotic and negative symptoms and comorbid substance abuse and improving social functioning and user satisfaction. The results of the OPUS-trial will be presented together with meta-analyses based on similar trials. The implementation of OPUS all over Denmark will be presented together with the Danish OPUS-fidelity study. Specialized elements are being are being developed such as inclusion of new methods in CBT for psychotic and negative symptoms, neurocognitive and social cognitive training programs, interventions for supported employment and focus on physical health. Results of long term follow-up studies indicate that the prognosis of first episode psychosis is very diverse with the extremes represented by one group being well functioning and able to quit medication without relapse; and another group having a long term chronic course of illness with a need for support to maintain daily activities. The Danish TAILOR-trial–testing dose reduction versus maintenance therapy will be presented. It will be of immense value to be able to intervene in risk groups identified in the premorbid phase, and there are few examples of ongoing trial for children of parent with schizophrenia and bipolar disorder.