Polarity of affective tone has taken the role of the core defining feature of bipolar affective disorder (BAD) eclipsing Falret's and Kraepelin's emphasis on cyclicity and recurrence. Yet in many clinical cases polarity is lost in the course of time while cyclic recurrence persists for decades, completely disrupting patients’ lives. That's why true “mood stabilisation” aims not as much at reducing episode severity as at reducing episode number to a minimum.

On the neuronal level polarity could be envisaged as interplay between arousal and inhibition due to trans-membrane ion currents, either brief and adaptive or pathologically sustained. Cyclicity and recurrence could arise from permanent deficits in neuronal plasticity and resilience which are to a large extent under genetic control. The “mood stabilising” properties of different pharmacological agents are due to multi-level actions on the intracellular signal transduction pathways affecting the function of Gi and Go proteins, of some intracellular messengers (mioinositol, Bcl-2, ER stress proteins, MARKS, the complex calmodulin-synapsin1-synaptotagmin), and of some crucially important enzymes: adenilyl cyclase, various protein kinases (ά, ε, C, MAP, Akt), mitochondrial respiratory chain enzyme complexes, histone deacetylase and acetyltransferase, GSK-3. Thus, in the long run “mood-stabilising agents” exert blockade of excitotoxic/apoptotic pathways, phosphorilation of microtubular proteins, and regulation of the expression of genes implicated in processes involved in neuroplasticity, neuroprotection, even neurogenesis, and hamper the long-term neuronal (and by extension, mental) deterioration. Lithium displays the broadest spectrum of such actions and provides, by far, the best control over the chronic protean symptoms of BAD.

According to recent knowledge there are probably multiple susceptibility genes involved in patophysiology of schizophrenia and bipolar disorder, each of small effect, which act in conjunction with environmental factors. These genes could influence synaptic plasticity, neurodevelopment and neurotransmission. There are an estimated 4,000 genes involved in the complicated communication between brain cells. However, overlapping of candidate genes between both disorders was reported.

Recent studies revealed that random mutations not inherited from either parent play a role in schizophrenia. The relation between psychopathological events, the phenomenology of the trauma and neurobiological changes related to schizophrenia and bipolar disorder is not totally understood.

The symptoms of schizophrenia are believed to be triggered by stress-induced changes in neurobiological systems representing an inadequate adaptation of neurobiological systems to exposure to stressors. Recent studies suggest that epigenetic mechanisms may play an important role in the interplay between stress exposure and genetic vulnerability also in humans. In preclinical studies it was first suggested that epigenetic mechanisms may be involved in the modulation of gene expression in response to stressful stimuli. Recently, epigenetic differences in a neuron-specific glucocorticoid receptor (NR3C1) promoter between postmortem hippocampus obtained from suicide victims with a history of childhood abuse and those from either suicide victims with no childhood abuse or controls were found, indicating the involvement of these mechanisms in human adaptation to stress. Future research could lead to prenatal screening for both disorders, and for new, more personalized approaches to treating people depending upon their genetic profile.

Oxytocin (OT) is an evolutionarily conserved nonapeptide that is produced in the magnocellular neurons of hypothalamic paraventricular and supraoptic nuclei. The widespread intracerebral projections of OT-producing neurons subserve its role as a neurotransmitter and neuromodulator. OT is well known for its functions in reproduction, including parturition and lactation. In recent years, the effects of OT on social interaction have become a focus in both normal and abnormal psychology research. OT attenuates fear responses, improves empathy and also exerts major effects on pair-bonding and attachment.

Studies have revealed that polymorphic variation of the oxytocin receptor gene (OXTR) also influences stress reactivity and empathetic responses in humans, as well as temperament, and even amygdala volume. This clearly implies that OXTR variation interacts with environmental contingencies, such that it can be regarded an interesting target in psychopathology research.

OT has the potential to ameliorate symptom severity in psychiatric conditions such as social anxiety disorder, autism and schizophrenia. Accordingly, future research into the interaction between OXTR variation and environment may contribute to clarify the role of OT in psychopathology.

The general medical model explains that there are genetic and environmental risks and protective factors in the aetiology of any complex disease. The main idea supported by this model is the existence of good and bad polymorphisms. We present a review of the literature and some examples of our own empirical studies about this issue in psychiatry; with special focus on the methodological problems of this medical model.

In relation with 5-HTTLPR we present the results of a longitudinal study of 1804 women. In this study the “LL” genotype seems to be a risk factor for post-partum depression, probably due to gene-hormone interaction after delivery. But the same genotype might be a protective factor of emotional disorder in other life-time and environmental condition.

In relation with COMT gene, we present a meta-analysis (including our own data) of 51 studies comprising 13,894 schizophrenic patients and 16,087. We found a small but significant protective effect for heterozygosis at rs4680 (pooled OR ¼ 0.947, P¼ 0.023; pooled OR ¼ 0.813, P¼ 0.0009). Thus, the COMT functional polymorphism rs4680 contributes to schizophrenia genetic susceptibility under an over-dominant model, indicating that both too high and too low levels of dopamine (DA) signalling maybe risk factors.

In summary, both examples suggested that there are no ‘bad’ or ‘good’ genotypes in relation to common variants. The controversial results of many genetics associations’ studies in psychiatry might become comprehensive under an evolutionary approach.

Delirium in patients older than 70 years is a frequnet problem on somatic wards in the general hospital, leading to adverse events such as falls, and/or prolonged length of hospitals stay.

Albeit c-l-psychiatrists and geriatricians since long have advocated the necessitiy to improve this situation, nothing really happens.

This lecture discusses problems, perils and pitfalls of this unsatisfying situation and tries to answer questions such as whether guidelines could be of help here, and whether pilot projects could be useful to lead the field further. The latter issue will be illustrated with two examples from Germany.

Concerning aging society problem of dementia is getting more and more significant. The causes of Alzheimer Disease (AD) are still not well known. The potential role of diet in the prevention of dementia including AD arouses increasing interest. Poly-unsaturated fatty acids (PUFA) are essential for brain growth and development playing an important role as critical modulators of neuronal function and regulation of oxidative stress mechanisms, in brain health and disease. Behavioral research studies with animals proved that ω-3 acids have antioxidant protection on neurons during pathogenesis of AD. DHA diet supplementation in animal models proved that ω-3 acids have positive influence on memory, attention, concentration and locomotor abilities in battery of tests such as 5/9 choice, X- or T-maze and activity wheel. DHA is obtained mainly through dietary intake being not produced by mammals, whereas DHA makes up 60% of fatty acids building neuronal cell membranes. These acids have beneficial effect on cardio-vascular system and may also reduce pathology processes of dementia diseases other than AD. Updated scientific data of ω-3 acids dietary intake in elderly will be presented and discussed.

Depression contributing to cardiovascular disease is a major clinical problem both due to frequent occurrence and serious health effects. Studies confirm a relationship between depressive disorders and risk for the development and unfavorable course of coronary artery disease (CAD) and myocardial infarction.The aim of the study was to assess how the comorbidity of depressive symptoms and CAD influences the quality of life (QoL) in patients after the successful coronary angioplasty (PCI). 227 patients with CAD selected for PCI were enrolled. 156 patients with full clinical and angiographic success and without restenosis within 4 weeks after the interventions were included in one year follow-up. Patients’ status was assessed four times (one day before and at 1, 6 and 12 months after the intervention). Polish version of SF-36, Beck Depression Inventory (BDI), Rosenberg's Self-esteem Scale (RS), Beck's Hopelessness Scale (HS) and Authomatic Thoughts Questionnaires (ATQ) were used.In the whole group QoL after one months after PCI was significantly improved. This tendency persisted in further examinations. There was a significant correlation between SF-36, which measures QoL, severity of depressive symptoms (BDI) and parameters describing depressive thinking style (HS, RS and ATQ). The presence of depressive symptoms at each assessment during follow-up, was associated with the poorer quality of life.Presenting study indicate that depressive symptoms in patients with coronary artery disease significantly affect the quality of life, despite of the successful coronary angioplasty. Optimized comprehensive approach to CAD patients may require psychological assessment and inclusion of adequate psychological or psychiatric interventions.

In Germany, the Forensic Hospital in Haina/Germany has a tradition of more than two decades of continuously outpatient treatment of mentally ill offenders. In our system, patients were conditionally released after a successful hospital order treatment. Time under parole for these patients normally spread between two to five years. In nower days, after a reform of penal law, time under parole can be unlimited.

Since 1988 far more than 1000 patients were released from the forensic hospital and treated under parole conditions in the community.

The paper will describe the careers of these patients, demonstrate rates of success and failure, and explain our treatment and risk-management approach.

Depending on the subject of the evaluation different outcome measures are necessary. Generally recidivism rates are considered to be state of the art in the assessment of forensic therapy effectiveness. In this context, recidivism can be defined differently. Thus a definition may include only new convictions for a specific type of offense or any offense or may even include new charges as well. In the evaluation of sex offender treatments it is often considered to be self-evident to define recidivism as a reconviction or new charge for a sex offense. Some authors however argue - not without reason - to include any type of violent offense in the definition. The evaluation of treatment effectiveness suggests however, also including therapeutic criteria such as level of openness of the patient. Especially openness about sexual fantasies relevant to the sex offense may be a key factor in the treatment of sex offenders. It is suggested that future research in the area include such ‘softer’ criteria as well.

The presentation will cover 3 aspects of reality:

1. 1) Reality as resistance;

2. 2) Reality as actuality;

3. 3) Reality as correct insight.

   A brief consideration of the nature of these in normals will be given.

1. a) undue resistance in depressive illness;

2. b) qualitative differences in actuality, i.e experience of external world and body in schizophrenia;

3. c) so-called “depressive realism” as a more correct insight into ones owen actions than is possessed in normals.

The medical model approach in Psychiatry brought up pressure for clear descriptors in diagnostic procedures. This presentation will address two particular psychopathological phenomena, described from the viewpoint of the observer and considered to be key psychotic features: patients’ “loss of contact with reality” and “bizarre” attribute of the content of the delusional phenomena. Challenges seem to occur from present hermeneutical, epistemological and conceptual limitations. Relevant to this is the practical impossibility to fully access a patient frame of reference and our (psychiatrists) subjective knowledge of the world, leading to a value-laden analysis of patients. We’ll be analyzing the historical, cultural and linguistic background and stressing the relevant links to the current psychiatric phenomenology.

The validity of both descriptors, used in classification systems, seems questionable as we find a practical impossible to represent those ways of experiencing, and something remaining unsurpassable, not understandable and inapprehensible. But if we find no consistent judgment in these psychopathological signs and remain confortable with frequent biases in clinical findings that do occur, then the weakness of both descriptors raises ethical problems. This presentation aims to suggest clues to an unbiased use and conceptualization of both. But a vital conclusion is that the gap between inner/subjective reality and objectively valuable and classifiable experience is perhaps beyond epistemic and constituent of personhood.

Drug abuse is able to modify the state of consciousness and, as a consequence, the sense of reality. The author describes two fundamental modifications of the sense of reality under drug effect: “floating” and “frozen”. The first, “floating” is induced by acute intoxication; the second, “frozen”, is produced by chronic drug dependence. These two reality modifications are described from a phenomenological and a psychopathological perspective. Intentionality, space, time, otherness are described in their different “floating” and frozenstructure. “Floating” patients need of adaequate medical treatment. In conclusion, the author introduces the dasein-group treatment, based upon shared emotions, as a concrete possibility to cure frozen patient.

Negative symptoms of schizophrenia have often been associated with poor functional outcome and poor response to antipsychotic treatment. Studies reporting drug induced significant reduction of negative symptoms after treatment actually refer to negative symptoms secondary to positive, depressive and/or extrapyramidal symptoms. Negative symptoms that do not improve following antipsychotic treatment represent a real challenge for future development of effective treatments. Two approaches have been so far proposed to improve research on these negative symptoms. The first one is based on the identification of primary and enduring negative symptoms, that characterize a schizophrenia subtype known as deficit schizophrenia (DS). The prevalence of DS is 15%–20% in population based samples, but tends to be much lower in first-episode patients. Individuals with DS have worse long-term outcome and poorer response to antipsychotics than those with other forms of schizophrenia. The second approach is based on the identification of persistent negative symptoms, which are likely to be primary, but may be secondary. Few data are available on the prevalence of persistent negative symptoms in patients with schizophrenia. In first episode subjects from the EUFEST study 11% of the study sample showed persistent negative symptoms (PNS). They had poorer functional outcome and lower remission rates than those without PNS after 1 year of treatment. Research on clinical and biological correlated of primary and/or persistent negative symptoms might help in reducing schizophrenia heterogeneity and developing new treatments.

The deficit syndrome defines a subgroup of schizophrenia patients with prominent and enduring primary negative symptoms (1). Behavioral, structural, and functional neuroimaging studies have implicated mainly the dorsolateral prefrontal - thalamocortical circuit. Deficit syndrome patients seem to have larger ventricles in MRI studies (2). Neurological soft signs suggest parietal involvement with greater sensory integration impairment in deficit syndrome patients (3). On the contrary, some biological markers such as P50 gating have not shown any difference between deficit and non-deficit schizophrenia (4). Finally, no pharmacological treatment has so far proven effective for the treatment of primary enduring negative symptoms (5). In conclusion, deficit pathology in schizophrenia seems to involve the prefrontal and parietal lobes and have different neurobiological substrates than positive symptoms.