The DSM diagnostic criteria of sexual dysfunctions have been widely used by clinicians, researchers and in pharmaceutical trials. However, these diagnostic criteria do not reflect the developments in the field of sexual medicine. These criteria are vague and do not include many of the criteria used in other mental disorders classified in the DSM. Better defined operational criteria are needed to define more homogenous population samples and to help answer some basic research questions.

Some of the issues that need to be addressed in the new revision of the sexual dysfunctions diagnostic criteria include the duration of sexual dysfunction, intensity and frequency of sexual dysfunction, the use of distress as a diagnostic criterion, whether there are specific differences in diagnosing female and male sexual dysfunction, validity of some diagnostic entities (e.g., sexual aversion disorder), reclassifying some sexual dysfunctions (e.g., dyspareunia as a pain disorder), and the overlap of diagnoses.

Further deliberation of sexual dysfunction classification should also include two core questions: a) when does a sexual problem become a sexual dysfunction, and related to that b) what do we consider “normal” and/or what is a biological variation of sexual functioning (e.g., are rapid ejaculation and extremely delayed ejaculation dysfunctions or normal variants of sexual performance at the very ends of the spectrum?).

This presentation will review in detail the deficiencies of the standing diagnostic criteria and will provide suggestions for improvement of these criteria based on evidence from the literature and on recommendations of expert panels.

There has been considerable research concerning the epidemiology and treatment of female sexual dysfunction. Research has indicated a high prevalence of female sexual problems in most cultures. Clinical trials have tested the efficacy of a variety of pharmaceutical agents for the treatment of female sexual dysfunction. This research can be grouped into three major areas: the use of hormonal agents, the use of centrally acting compounds and the use of agents promoting peripheral vasodilation. This presentation will review current research, treatment options, and gaps in our knowledge.

Drug treatment of lifelong premature ejaculation (PE) consists of daily use of SSRIs, particularly paroxetine 20mg and sertraline 50-100mg, on-demand use of clomipramine 20-50mg (3-6 hour prior to coitus) and/or topical anesthetics, such as lidocaine and prilocaine [1].

PE is a common male sexual complaint in approximately 20-40% of men. However, not all these men require treatment. PE has been distinguished in Lifelong and Acquired PE. Recently, two other PE syndromes have been classified [2,3]. In “Normal Variable PE” the occurrence of early ejaculation is rather inconsistent and should be regarded as a normal pattern of ejaculatory performance [2]. In “Premature-like Ejaculatory Dysfunction” men complain of an early ejaculation while the duration of the IELT is in the normal range (about 5 minutes) or even longer (5-10 min) [3]. The four PE syndromes require different forms of treatment. Lifelong PE should be treated with medication. Acquired PE needs medication and/or psychotherapy. Normal Variable PE requires psycho-education and Premature-like PE requires either psychotherapy, psycho-education or counselling.

Although a series of DNA-sequence variants in proposed disposition genes for schizophrenia have been identified, the mechanisms to translate the genetic vulnerability for schizophrenia to the manifestation of the disease remain obscure. The analysis of the relationship of disease-associated alleles and combinations of alleles (haplotypes) to the clinical features and associated neurobiological correlates offer a tool to increase our understanding of the aetiology of schizophrenia.

We will explore this relationship in a series of case-control samples by (1) extracting schizophrenia-associated alleles and haplotypes of postulated susceptibility and modifying genes, (2) testing these identified genetic markers for association with neuropsychological and neuroimaging features of schizophrenia.

Abstract not available at the time of printing.

Cannabis use has been related to many psychiatric problems, particularly psychotic disorders, affective disorders, and anxiety. Chronic cannabis use is related to panic attacks, anxiety, depression, and low motivation. It would appear that frequent cannabis use during adolescence is predictive of later depression and anxiety. Cannabis has also been related to amotivational syndrome in chronic users. This disorder is characterized by a personal deterioration with loss of energy and work drive, but the validity of this syndrome remains uncertain. Epidemiological studies have shown a clear association between cannabis use and psychosis, mainly adult schizophreniform disorders. Recent studies have identified a higher frequency of disturbance in sensorium, irritability, affective disturbances, derealization/depersonalization, and visual hallucinations in cannabis induced psychosis than in acute schizophrenia psychosis. Schizophrenia with substance abuse has been associated with poor treatment compliance, increased rates of hospital admissions, suicide, violent behavior and unstable housing and homelessness. Cannabis use specifically has been correlated with the exacerbation of psychotic symptoms and increased tardive dyskenisia. It may be the case that schizophrenic patients are inclined to consume cannabis, either due to lowered impulse control or as a means of reducing negative symptoms. On the other hand, it may be that cannabis use itself either causes of precipitates psychosis. In short, the association between cannabis use, psychosis, depression, behavioral problems, tobacco smoking, excessive drinking and use of illicit drugs shows a severe pattern of comorbidity that may lead to further negative outcomes, and requires further study for the identification of appropriate treatments.

The endocannabinoid system has been involved in a variety of physiological functions, including the control of nociception, motor behaviour, learning/memory, reward, neuroprotection, food intake and metabolism. This system is mainly activated in response to external stimuli to help stablish the steady-state homeostasis of other neurotransmitters and mediators. Recent studies have involved the endocannabinoid system in the common neurobiological substrate underlying drug addictive processes. This system participates in the primary rewarding effects of cannabinoids, nicotine, alcohol and opioids through the release of endocannabinoids in the ventral tegmental area. Endocannabinoids are also involved in the motivation to seek the drug by a dopamine-independent mechanism demonstrated for psychostimulants and opioids. The endocannabinoid system participates as well in relapse to drug-seeking behaviour by mediating the motivational effects of drug-related environmental stimuli and drug re-exposure. In agreement, clinical trials have revealed the effectiveness of the CB1 cannabinoid antagonist rimonabant to obtain smoking cessation. CB1 cannabinoid antagonists could represent a new generation of compounds to treat drug addiction.

Dopaminergic system within mesocorticolimbic circuit plays a crucial role in addictive behaviors. However, no data to date are available concerning the effect of cannabis addiction on dopaminergic neurotransmisson in humans. The neuronal dopamine transporter (DAT) ensures the regulation of dopaminergic neurotransmission by the re-uptake of extracellular dopamine. Observation of DAT density anomalies within the mesocorticolimbic system in cannabis-dependant subjects could provide further evidence for the implication of dopaminergic dysfunction in cannabis addiction. Thus, this work aims at the study of DAT density in control, tobaccos-dependents subjects and cannabis-dependants subjects, gender and age-paired with Positron Emission Tomography (PET).

Subjects are scanned on High Resolution Research Tomograph (HRRT) for one hour after injection of a selective DAT radioligand ([11C]-PE2I). The binding potential (BP) in regions of interest previously defined within the mesocorticolimbic circuit was calculated using a simplified reference tissue of Lammertsma in order to measure an index of DAT density. BP-obtained in each group: control, tobacco-dependents and cannabis-dependents subjects, were compared with t-tests. Preliminary results will be presented during the seminar.

Abstract not available at the time of printing.

In recent years, social cognition became a valuable construct for understanding the nature and disability of schizophrenia (Green et al, 2005), and different studies have pointed out for its potential as a mediator of relations between neurocognition and functional status in schizophrenia (Sergi et al, 2006).

This presentation aims to review the concept of social cognition, describe the key social cognitive domains, discuss the importance of social cognition in schizophrenia by highlighting its functional significance, and finally present a brief overview of the main methodological issues regarding research on some of the presented issues.

Social cognition appears to be an important mediating factor between cognitive and social functioning in schizophrenia which may increase the efficacy of different cognitive-behavioural therapies. In fact, social cognition is becoming a specific target of these interventions, including psychoeducation, cognitive remediation, social skills training and cognitive therapy for positive symptoms. By means of a systematic literature review, main publications about possible efficacy of social cognition in four major languages (English, Spanish, French, and German) are selected. According to this review, main empirical results concerning therapy of social cognition in schizophrenia, both in research and clinical settings, are shown in this presentation. Finally, some practical recommendations about these therapies are provided.

There is general consensus that social cognition is a key cognitive dysfunction in schizophrenia. At the same time, the hypothesis that social cognition is an aspect of cognition that determines social functioning has been receiving more and more empirical support since it was first proposed a few years ago.

However, the actual definition of “social cognition” can be a confounding factor in this framework. The definition has been a matter of debate in literature and only recently has some consensus emerged about the aspects that constitute “social cognition” (emotion perception, theory of mind, social perception, attributional style, social scheme). As a consequence, most of the time research in this area only considers some of these aspects, probably because the instruments available to measure social cognition measure these aspects individually and not social cognition globally.

The SCS (social cognition scale) is an instrument under development with the goal of measuring together some of the components of social cognition, specifically: identification of stimuli, emotion perception, and social perception. Results show that the social perception of the patients who participated in the social perception program has improved. Patients that have received training in social perception learn to gather more information from an image, and to make more adequate interpretations.

During the past two years we designed a cognitive-behavioural group therapy program (INT) as further development of the cognitive part of Integrated Psychological Therapy (IPT). INT is partly computer based and intends to restitute and compensate neuro- and social cognitive (dys-)functions. The program is embedded in the daily living context of the patients and starts from their resources with a special focus on facilitating intrinsic motivation. The INT-manual contains exercises to improve the following (MATRICS) areas: Speed of processing, attention/vigilance, verbal and visual learning and memory, working memory, reasoning and problem solving, emotional and social perception, social schema and emotion regulation.

Currently we evaluate INT in a randomized multi-centre study in Switzerland and Germany. INT is compared with TAU. Outpatients with a diagnosis of schizophrenia (DSM-IV) are included. Assessments are applied before and after therapy with a 1 year follow-up. Additionally the therapy process is evaluated. Assessment instruments measure neuro- and social cognition, psychopathology, social functioning, quality of life, expectation of self-efficacy and therapy motivation. Patients receive 30 therapy sessions each lasting 90 minutes for 15 weeks. During the first study year 44 patients participated (23 for INT and 21 for TAU groups). First results (pre- post assessments) show better outcome of INT patients in neurocognitive variables, emotion perception, self-rated motivation and self-efficacy. Up to now we didn't find a significant influence on social functioning and on psychopathology. Further results, especially data of the follow-up have to confirm the significance of the newly developed therapy program within other rehabilitation approaches.

The workshop deals with various aspects of the provision of psychiatric services in Europe in general and in selected European countries.

The differences in the provision of psychiatric care between East and West will be highlighted and the need to channel the recommended action in an appropriate need – centered way is emphasized. Other challenges in the provision of psychiatric services will also be dealt with.

The advances, the challenges and the problems in mental health provision in selected European countries in East and West (Serbia, Germany and France) will be presented under the light of recent developments in these Countries (e.g. the new French Mental Health Plan).

Special emphasis will be given to the difficulties in the transition from Mental Hospital Psychiatry to community care and to the ethical aspects of this transition.

Patients with health-anxiety are very often unable to describe concrete consequences of their putative somatic diseases. They block their thoughts due to anxiety attended this thoughts. The health-anxious patients try not to think about illness at all, by attempting to control their thoughts or by distraction. Our method is based on therapeutic dialogue, using Socratic questioning, and inductive methods which force patient to think beyond actual blocks.

In second step, patients are asked to think out all other possibilities of newly discovered future. They are forced to imagine the worse consequences of all dread situations. Dialogue is led through one's serious illness status, with its somatic, psychological and social consequences, and the dying experience to the moment of death, which has to be described with all related emotions and details. Further, we ask patients to fantasize and constellate possible “after death experiences”. In the next session the patient brings a written conception of the redoubtable situation previously discussed. Than we work with this text as in imaginative exposure therapy.

This method seems to be quite effective and not too time-consuming. Several patients with health-anxiety underwent this exposure in our therapeutical groups. All of these patients profited from this therapy, as confirmed by follow-up data.

Participants will learn:

1. • conceptualization of health anxiety with the patient;

2. • Socratic questioning with the hypochondriacal patient;

3. • how to apply the exposure to the imaginative death experience.

Supported by the research project No. 1M0517 from Ministry of Education, Youth and Sports, the Czech Republic.

The administration of inert treatments along with verbal suggestions of either clinical improvement (placebo) or worsening (nocebo) are known to powerfully affect the course of some symptoms and diseases. In fact, placebos and nocebos have been found to affect the brain in different conditions, like pain, motor disorders and depression. It has also been shown that this may occur through both cognitive factors, like expectation, and conditioning mechanisms. In recent years, placebo- and nocebo-induced expectations have been analyzed with sophisticated neurobiological tools that have uncovered specific mechanisms at both the biochemical and cellular level. For example, positive expectations (placebos) have been found to activate endogenous opioids whereas negative expectations activate cholecystokinin. Placebos have also been found to induce a release of dopamine in the striatum and to affect the activity of single neurons in the subthalamic nucleus in Parkinson patients. There is also experimental evidence that different serotonin-related brain regions are involved in the placebo response in depression. Recently, the placebo effect has been studied with a different experimental approach, in which hidden (unexpected) medical treatments were carried out and compared with open (expected) ones. In all cases, the hidden medical treatments were less effective than the open ones. These findings show that the patient's awareness about a therapy is of crucial importance in the therapeutic outcome. Overall, all these studies show that the psychosocial context around the therapy, particularly the doctor's words, may induce changes in the patient's brain that, in turn, may affect the course of a disease.

Recent neuroscientific evidence has revealed that the adult brain is capable of substantial plastic change in areas that were formerly thought to be modifiable only during early experience. These findings have implications for our understanding of chronic pain. Functional reorganization in several brain areas related to the processing of pain was observed in neuropathic and musculoskeletal pain. In chronic low back pain and fibromyalgia patients the amount of reorganizational change increases with chronicity, in phantom limb pain and other neuropathic pain syndromes cortical reorganization is correlated with the amount of pain. These central alterations may be viewed as pain memories that influence the processing of both painful and nonpainful input to the brain. Learning processes that contribute to the development of pain-related memory traces are predominantly implicit and involve processes such as sensitization, operant and classical conditioning or priming. Cortical plasticity related to chronic pain can be modified by behavioral interventions that provide feedback to the brain areas that were altered by pain memories. These behavioral interventions can be enhanced by pharmacological agents that prevent or reverse maladaptive memory formation.

At the Ministerial Conference of the European Office of the WHO the Helsinki declaration was endorsed by all member states of the European Region. The Declaration offered a vision of a comprehensive and inclusive scope of mental health activities. Since then many countries have drafted or scrutinised strategies according to the declaration and activities have been developed in areas ranging from anti-stigma and suicide prevention strategies to the improvement of facilities, development of services and community activities.

There have been numerous successes, but we have also become aware of challenges which need addressing in a variety of ways. These include the absence of evidence in some crucial areas, the cost of service development, health systems not suited to the demands of mental health care, workforce challenges and the stigma and discrimination experienced by users, carers, services and staff.

AEP is an organization based on individual membership of those working in the field of mental health care and research in Europe. The role of AEP is changing hand in hand with the harmonization process in European policy including the mental health. The activity of the association as well as the participation of its individual members representing different parts of Europe is to some extent parallel and complementary to the official programs on mental health (WHO a EC projects, STAKES, IMPHA etc.). In addition, there is a significant overlap with such programs, which will be briefly summarized in the forum.