Medicine as a discipline cannot function in a social or cultural vacuum. Culture and society determine what is pathological or deviant and where help is sought from. Society and cultures also determine child rearing patterns and cognitive schema as well as the way we learn to look at the world-developing our world view whether that is related to medicine or society as a whole. The reductionist view in medicine is that medicine as a discipline relies on biological factors. However, it is often ignored that biology itself is affected by social and cultural factors including diet, attachment patterns, use of substances etc. Society dictates the type of medicine being practised and the resources that are made available. It is the members of society directly or through stakeholders who determine what sources are needed for training of health care professionals across all medical disciplines. In addition, especially in psychiatry, the society will determine and dictate deviance and how deviance is to be dealt with along with what is seen as risk behaviour and who determines the severity and who deals with it. The concept of the social contract originally between the monarchs and their subjects dates back centuries and is simulated between physicians and society as a whole. However this is implicit and not explicit and is negotiated between the stakeholders and the health care professionals. Stakeholders also determine and dictate how the professions are regulated. It is the regulatory bodies to whom the physicians answer regarding their clinical practice and standards of health care delivery. Certain aspects of clinical medicine will always be social and be very strongly influenced by prevalent social factors. These can be applied to causative or contributory factors as well as in the intervention and management strategies. Furthermore, for certain psychiatric conditions cultures and societies play a major role in moulding the symptoms, identifying idioms of distress and defining illness and sickness behaviours. This action is social and dictates what is seen as normal and what is seen as abnormal.

The new century brings with it new tasks and challenges for social psychiatry. These include the tche development of research and practice bridging of the gap between social psychiatry and the other disciplines of psychiatry; need for a focused effort to understand the impact of new communication technology on mental health and illness; the consequences of the longer life expectancy of people with chronic mental illness for those ill and for society; the impact of significant changes of the concept of family and inter-human responsibilities on social capital; the consequences of the constant lowering of the threshold of suffering in populations of; and numerous others.

The Kraepelinian dichotomy posits that patients with schizophrenia (SCZ) and bipolar disorder (BD) present as two separate psychotic entities such that they differ in terms of clinical severity including neurocognitive functioning. Based on clinical impression within a tertiary psychiatric hospital context and extant data, we hypothesized that patients with SCZ had a similar level of neurcognitive impairment compared with BD. Forty-nine healthy controls (HC), 72 SCZ and 42 BD patients who were matched for age, gender, and premorbid IQ were administered the Brief Assessment of Cognition battery (BAC), the Positive and Negative Syndrome Scale for SCZ patients, the Young Mania Rating Scale (YMRS) for BD patients, and Global Assessment of Functioning (GAF) for both patients groups. Both BD and SCZ groups demonstrated similar patterns of neurocognitive deficits across several domains (verbal memory, working memory, semantic fluency, processing speed) compared with HC subjects. However, no significant difference was found in neurocognitive functioning between BD and SCZ patients, suggesting that both patient groups suffer the same degree of neurocognitive impairment. Moreover, patients with lower level of psychosocial functioning as indicated by lower GAF score (F(1,112) = 2.661, p = 0.009) and older age (F(1,112) = −2.625, p = 0.010), not diagnosis or doses of psychotropic medications, predicted were associated with poorer overall neurocognitive functioning as measured by the(lower BAC composite score). Our findings of comparable neurocognitive impairments between SCZ and BD affirm our hypothesis and support less the Kraepelinian concept of dichotomy but more of a continuum of psychotic spectrum conditions.

Abnormalities in glutamate signaling and glutamate toxicity are thought to be important in the pathophysiology of bipolar disorder (BD). Whilst previous studies have found brain white matter changes in BD, there is paucity of data about how glutamatergic genes affect brain white matter integrity in BD. Based on extant neuroimaging data, we hypothesized that GRIN2B risk allele is associated with reductions of brain white matter integrity in the frontal, parietal, temporal, occipital regions and cingulate gyrus in BD. Fourteen patients with BD and 22 age, gender, handedness matched healthy controls were genotyped using blood samples and underwent diffusion tensor imaging. Compared to G allele, brain FA values were significantly lower in BD patients with risk T allele in left frontal region (p = 0.001), right frontal region (p =0.002), left parietal region (p = 0.001), left occipital region (p = 0.001), right occipital region (p <0.001), left cingulate gyrus (p = 0.001). Further elucidation of the interactions between different glutamate genes and their relationships with such structural, functional brain substrates will enhance our understanding of the link between dysregulated glutamatergic neurotransmission and neuroimaging endophenotypes in BD.

The causes of why certain people engage in suicidal behaviors involve both environmental and genetic factors, and interactions in-between. The aim here was to study certain aspects of stress-vulnerability in SA, i.e. the association of polymorphisms in genes which e.g. regulate the neuroendocrine hypothalamic-pituitary-adrenal (HPA) axis stress-response, as well as the importance of gene-environment interactions (GxE).

We studied genetic associations in the context of parent-child inheritance, as well as gene-environment interaction (GxE) patterns considering life timing of trauma and gender, concerning polymorphisms in candidate hypothalamic-pituitary-adrenal (HPA) axis gene networks, as well as on a genome-wide scale. For GxEs, we assessed exposures to physical assault (PA, below or over age of 18) or cumulative, lifetime exposure to a panel of stressful life events (SLEs) in male and females. Studies were conducted by a family-based design (n=660 trios) in relation to the outcome of severe lifetime SA in the offspring.

We have previously shown the associations of several HPA-regulatory candidate genes. The current results aim to present an extension involving more genes and make an attempt to shift towards polygenetic associations, which may lead to a better understanding of etiology. We investigate the patterns of GxE vs non-GxE associations, with the aim to better define the genetic components of the stress diathesis model for suicidal behaviors.

Personalised approaches have a long history in the treatment of alcoholism. ‘Matching treatments to patient's heterogeneity’ was the codeword for these attempts. Large studies failed to show a matching effect, maybe because they only took behaviour and psychophathology as basis for matching. More recent studies included biological variables for stratification of patients. Genetics, neuroimaging and psychopathology showed very promising results. Examples of the PREDICT study (Mann et al., 2013) will be given.

424 patients were randomised to either placebo, naltrexone or acamprosate. Using neuroimaging we confirmed that an increase in brain activity in the ventral striatum is related to time to relapse. We also found support for our hypothesis concerning the rewarding characteristics of alcohol in a certain subgroup of patients. Here f-MRI BOLD response in the ventral striatum predicted a positive naltrexone response. Finally a psychometric test distinguished between ‘reward cravers’ and ‘relief cravers’ (Glöckner-Rist et al., 2013).The former respond significantly better to pharmacotherapy.

In conclusion the treatment of alcoholism is moving towards a personalised approach. This holds the potential for a significant increase in effect sizes of our treatment trials and thus for better treatment options for our patients.

Mood disorders, including depression and bipolar disorder, have a strong familial basis and unaffected offspring of affected individuals have a substantially increased lifetime risk of these and other psychiatric disorders. It is increasingly understood that risk is conferred through the cumulative effects of a number of common genetic variants each of low-effect size. Using data from the Psychiatric Genomics Consortium, we conducted polygenic risk profiling of cohorts of individuals with brain imaging (Bipolar Family Study) and/or cognitive data. We showed that increased polygenic risk of mood disorder is associated with functional abnormalities of ventral prefrontal limbic areas and with reduced connectivity, measured using diffusion tensor imaging (DTI). We discuss the utility of polygenic profiling for biomarker and mechanism discovery and its potential role in predicting disease-associated phenotypes and clinical illness.

Changes taking place nowadays, such as globalisation, increased mobility, population ageing, financial crisis and social networking force us to test the old views and adapt to the new realities. This consequently leads to interrogations that reflect current differences of perception created by the great velocity and intensity, followed by an unprecedented degree of interconnectivity and lowering of international barriers.

Therefore, it is worthwhile to look for actual and future migration onto the new global context by recognizing the push factors that pressure people to leave the donor country, the pull factors that make the recipient country seem attractive, while confirming patterns and duration of migration. Despite the concern for migration has moved to the forefront agendas raising questions, nevertheless, there is lack of data of migration flows, as significant highly skilled migration has been within the European Union, and additionally, there is scarcity of data in psychiatry.

For that reason, as an attempt to explore migration among psychiatry trainees, the European Federation of Psychiatry Trainees (EFPT) has been doing a survey to assess opinions and experiences of international migration. This data analysis and discussion will permit further comparisons with other groups, such as physicians in general and psychiatry consultants.

The results provided by this study bring an overview of migration among psychiatric trainees and the different challenges faced in this pathway to a psychiatry career. Migration within psychiatry will probably continue, being therefore essential to enhance support to those who migrate, and actually influence the mental health care provided internationally.

Microglia express the TSPO (TranSlocalor PrOtein) receptor formerly known as the PBR (peripheral benzodiazepine receptor). The densitiy of the TSPO is dependent on the inflammatory state of microglia. The radiopharmaceutical [11C]PK11195 binds in excess to the TSPO in activated microglia. We showed that the hippocampus of psychotic patients experienced significantly more [11C]PK11195 binding than the hippocampus of healthy controls. To elucidate the effect of antipsychotic medication on brain inflammation the herpes encephalitis rat model was chosen, because of pathophysiological similarity: Herpes simplex virus preferentially infects hippocampus. In adult rats 10E5 pfu of HSV-1 (clinical strain) was administered intranasally. After 3–5 days sickness behavior developed. At the 6th day and at the 13th day after inoculation a [11C]PK11195 PET scan was performed. Drugs were delivered by osmotic minipumps (haloperidol, clozapine, saline). Only clozapine treatment delayed sickness behavior. Clozapine treatment reduced the inflammation in the mesecephalon and immediate surrounding regions after 6 days and reduced dissemination of inflammation to brain cortex at 13 days after inoculation.

Hypersexuality can be defined as an uncontrollable sexual behaviour that causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. These out-of-control sexual behaviours can be described as compulsive, impulsive, or addictive. Some authors argue that it serves to anesthetize feeling of pain, inadequacy, low self-esteem, social and personal phobias, isolation, and loneliness. Hypersexuality is conceptualized as primarily a nonparaphilic sexual desire disorder, but paraphilic sexual fantasies, arousal, urges, and behaviours can co-occur.

In the literature there is little evidence about a correlation between hypersexuality and sexual aggression. Even in a common risk assessment instrument, such as the SVR-20 (Sexual Violence Risk-20) manual, hypersexuality is not included as a risk factor for the assessment of sexual violence risk. However, the SAPROF (Structured Assessment of PROtective Factors for violence risk) manual has ‘a well developed self-control’ item as a protective factor against violence. It is obvious that people suffering from hypersexuality have developed no or poor self-control. Internalizing comorbid disorders are common in hypersexuality, but also externalizing comorbid disorders do occur.

In this paper, scientific evidence for the relationship between hypersexuality and sexual aggression will be reviewed. Next, clinical vignettes and data from a Belgian sex offender population (at the University Forensic Centre, Antwerp University Hospital) will be presented. and finally, the importance of this topic for caregivers in general and forensic psychiatry will be discussed.

Impairments of neurocognitive functioning were largely documented in patients with schizophrenia. These deficits have strong relationships with functional outcome and represent unmet needs of available treatments for schizophrenia. Studies on the efficacy of cognitive remediation (CR) targeting these dysfunctions produced encouraging results. In fact, several reviews and meta-analyses (1,2) and our own data (3) indicate that CR approaches determine improvements of cognitive functioning in patients with schizophrenia. An impact on functional outcome was reported more consistently when the CR program was combined with a psychosocial intervention, such as vocational rehabilitation or social skills training (1–4). The mechanisms underlying synergistic effects of combining CR with other interventions are not clear. At the moment, studies with an optimal design to address mechanisms of interactions between the two rehabilitation approaches are lacking. Our data on differential effects of the two programs on functional outcome suggested that programs integrating cognitive and social skills training might target a larger number of functional impairments, but should be planned carefully and individually to fully exploit the synergistic potential, while avoiding the interference of detrimental effects of one program component with the favorable impact of the other component.