Alcohol stimulates dopamine release and chronic intake is associated with neuroadaptation in the brain reward system. Previous studies described

1. 1) increased brain activation following the presentation of alcohol-associated stimuli, which was directly correlated with dopamine D2 receptor reductions in the ventral striatum, and

2. 2) a decreased response to stimuli that predict non-alcohol (e.g. monetary) rewards.

This alteration of brain responses to alcohol-associated versus non-alcohol cues may result from altered reward-associated learning in alcoholism. Indeed, alcohol-dependent patients displayed a decreased learning rate and performeance in a probabilistic reversal task. A brain imaging study revealed that the decreased learning rate was associated with impaired prefrontal-striatal connectivity during reward-dependent reversal learning. These results point to deficits in reward-associated learning, which contribute to alcohol craving. Since such reward-associated learning deficits can interfere with learning of new, non-alcohol associated behavior, cognitive behavior therapy may profit from taking such learning speed impairments into account.

The practice of electroconvulsive therapy (ECT) and the attitudes of psychiatrists towards ECT in the Chuvash Republic are described. A significant proportion of Chuvash psychiatrists had a patchy knowledge about ECT and held negative attitudes towards the treatment. Enhancing the knowledge about ECT and changing negative attitudes will require persistent educational efforts.

This study aimed to examine the association between the availability of firearms at home, and the proportion of firearm suicides in Switzerland in an ecological analysis. The data series were analysed by canton and yielded a fairly high correlation (Spearman's rho = 0.60). Thus, the association holds also at a sub-national level.

Stress can be defined as the subject's response - both emotionally and physically - to stimuli (stressors) from the environment. Stressors are not necessarily negative. They are, when they exceed the subject's ability to cope with them in a physiological way. This level of stress is indicated as pathological stress.

Addiction and pathological stress are strongly interrelated on several levels. Animal studies have shown that the pathological stress during the development may be the most important factor that brings the vulnerability for addiction to expression. Stress during pregnancy may have a decisive influence on brain development and the subject's ability to cope with stress during later life. Patients with post traumatic stress disorder have an increase risk for the development of substance use disorders.

The brain reward system is a major target for the central and peripheral stress system. The catecholamines that mediate the stress response play an important role in the development of addiction. Addictive drugs such as stimulantia act as stressors by activating stress hormons. The process of craving is strongly associated with activated stress systems. Therefore, the adequate treatment of substance use disorders requires interventions that reduce pathological stress for the patient, either by diminishing environmental stress or by increasing the ability to cope with stress.

Suicidal behavior runs in families and is prevalent in adolescence. Case-control and family-based studies in this age group failed to find a genetic association that survived replications. Gene environment approach gave new hope for possible associations especially with the short allele of the serotonin transporter promoter polymorphism (5-HTTLPR). However, a recent meta-analysis raised doubts about the consistency of these findings. Some new structural and functional imaging data may shade light on the age-related and gender-related development of the brain. This review suggests a new approach to gene by environment and timing interaction to understand the interplay that leads to suicidality in adolescents and young adults.

Major problems in treating patients suffering from addictions derive from the fact that the diagnostic category dependence syndrome covers a highly inhomogeneous patient group. Therefore uniform therapeutic approaches inflexibly following treatment guidelines have not fulfilled prognostic expectations. This was the starting point for developing a new modular resource-oriented treatment program in the Anton Proksch Institute Vienna.

Changing paradigms in the treatment of addiction, the Orpheus Programme offers a host of different modules designed to help patients to discover their own aims, objectives, values, and resources. The main task of the Orpheus modules is an increasing autonomous and joyful life. Abstinence represents no longer the only final goal of therapy, but is an important step to offer space and possibilities for the patients’ new life. When life becomes once again beautiful and filled with joy and meaning, addictive substances lose their seductive power: The more beautiful and attractive the patient's life, the less the drugs attractiveness. As illustrated by Orpheus, who defeated the sirens (as a symbol for addictive agents) by making the better, louder, and more attractive music, it becomes the patients’ main task to make a better “music of life”; the Orpheus modules are not training programs telling the patients how the better life looks like (as in former moral therapy); they intend to provide places, spaces and atmospheres encouraging and promoting the patients to make possible the possible.

Despite strong evidence for a role of biological factors in the etiology and pathology of suicide, the study of traditional neurotransmitter systems has been able to explain only a small proportion of the neurobiology of what is now recognized as a complex genetic trait. The use of microarrays to simultaneously examine the expression levels of thousands of gene transcripts has vastly expanded our capacity to detect the involvement of additional genes and pathways in suicidality, and has opened many new avenues for the discovery of the biological underpinnings of suicide completion. This review examines microarray studies which have been used to identify genes displaying altered expression in suicide completers, and highlights some of the important methodological considerations and metabolic pathways which have emerged from these analyses.

Pharmacogenetic influences on therapeutic response to e.g. antidepressant or neuroleptic treatment are poorly understood and the lack of efficacy in many of the patients together with side effects can both limit therapy and compliance. Thus the aim of pharmacogenetics and pharmacogenomics is to provide predictive tools for the response to psychopharmacologic agents in the therapy of psychiatric disorders and in that ways to provide a real personalized psychiatry. The following review will summarize the current stage of pharmacogenetics and pharmacogenomics and will critically discuss the possibilities of a personalized medicine.

Recent theories of addictive behaviors suggest that neurocognitive mechanisms, such as attentional processing, cognitive control, and reward processing play a role in the maintenance or development of addiction. Several studies will be discussed demonstrating the role of these neurocognitive mechanisms in addiction. Moreover, clinical issues such as the feasibility to use neurocognitive measures as predictor of treatment success and relapse will be discussed.

This paper presents a tentative typology of genetic and environmental pathways to suicidal behavior. Ten pathways are proposed and briefly illustrated: (i) direct effects from psychiatric disorders; (ii) direct effects from personality; (iii) direct effects of early adversity; (iv) direct effects of current adversity; (v) indirect effects of genes on selection into adversity (gene–environment correlation); (vi) interactions between genetic risk and current adversity: gene–environment interaction; (vii) interactions between early and current adversity: environment–environment interaction; (viii) interactions between culture and genes; (ix) dynamic developmental pathways involving causal loops from genes to environment and back again; and (x) gene × environment × development interaction.