We will propose a critical review of the scientific literature regarding pain and schizophrenia, examine the empirical basis for the reported pain insensitivity of schizophrenia, and emphasize the distinction between behavioral responses to pain or self-reported pain and physiological response to painful stimuli. Litterature is scarse and could be classified in 4 groups: case reports (n = 9), clinical studies (n = 23), experimental research (n = 20) and review articles (n = 5).

The analysis of Case reports and clinical studies show reduced pain reactivity in patients with schizophrenia compared to healthy controls or other psychiatric patients. In the same vein, experimental studies using self-report measures of pain reactivity generally reported higher pain perception thresholds in patients with schizophrenia. However, the only experimental study using a neurophysiological measure of pain reactivity (the nociceptive RIII reflex) demonstrated a normal pain threshold in schizophrenia.

Review of clinical and experimental data indicates that in most situations behavioral pain reactivity and self-reported responses to pain are reduced in schizophrenia. However, there is little or no physiological evidence supporting pain insensitivity in schizophrenia. It can be suggested that the widely accepted notion of reduced pain sensitivity in schizophrenia is related more to a different mode of pain expression than to a real endogenous analgesia. We will also present preliminary data on pain sensitivity associating behavioural pain reactivity measurements, "objective" electrophysiological assessments and neurovegetative function recordings. Our results are in the line of the literature and strongly suggest that there is no analgesia in schizophrenia but a different mode of pain expression.

Two study lines will be presented. One is focussing on the changes in experimental pain responsiveness in patients with dementia compared to healthy elderly and individuals with MCI. Patients with dementia appeared as more pain responsive (lower RIII-reflex thresholds, more pain-related facial responses, no difference in ratings) whereas the results of the MCI group were indistinguishable from those of the health elderly. Only the sympathetic skin response was similarly smaller in patients with dementia and the MCI individuals. The clinical reports of less frequent pain and less requirements of analgesics in dementia were not corroborated by the present experimental data. In the second study line, neuropsychological correlates of experimental pain sensitivity (rating, RIII-reflex, facial responses) were investigated in patients with MCI and dementia. The scores of a screening battery for dementia (SIDAM) and a modified version of the TMT-A were used. Significant correlations were found but only for the R-III threshold. Especially the scale for executive functions helped to explain the R-III reflex thresholds, suggesting frontal contributions to changes in pain processing in dementia. Depression, who often impacts pain processing, did not mediate the relationship between experimental pain and neuropsychology.

Although posttraumatic stress disorder (PTSD) is associated with chronic pain, preliminary evidence suggests reduced experimental pain sensitivity in this disorder. The questions addressed in the present study were whether pain perception would also be reduced in PTSD patients who are not suffering from chronic pain symptoms, and whether a reduction in pain sensitivity would also be present in combat veterans who did not develop PTSD. For this, we determined thermal detection and pain thresholds in 10 male combat-related PTSD patients, 10 combat control subjects (no PTSD) and 10 healthy controls without combat experience. All subjects were pain free. First, we measured thermal sensory thresholds with ramped heat and cold stimuli using the method of limits. Ramped thermal sensory stimulation revealed no deficits for the detection of (non-noxious) f2.1thermal stimuli between groups. In contrast, heat and cold pain thresholds in both combat groups (PTSD and combat controls) were significantly increased compared to healthy controls. However, these stimuli could not distinguish between the two groups due to ceiling effects. When using longer-lasting heat stimulation at different temperatures (30 s duration; method of fixed stimuli), we found significantly lower frequency of pain reports in PTSD patients compared with both combat and healthy controls, as well as significantly lower pain ratings. Our results suggest an association of PTSD with reduced pain sensitivity, which could be related to PTSD-related (neuro-)psychological alterations or to a pre-existing risk factor for the disorder.

Progress in unravelling the cellular and molecular basis of mammalian circadian regulation over the past decade has provided us with data that deteriorations in measurable circadian output parameters, such as sleep/wake deficits and dysregulation of circulating hormone levels, are common features of most central nervous system disorders.

At the core of the mammalian circadian system is a complex of molecular oscillations within the hypothalamic suprachiasmatic nucleus. These oscillations are modifiable by afferent signals from the environment, and integrated signals are subsequently conveyed to remote central neural circuits where specific output rhythms are regulated. Usually our sleep/wake cycle, temperature and melatonin rhythms are internally synchronized with a stable phase relationship. When there is a desynchrony between the sleep/wake cycle and circadian rhythm, sleep disorders such as advanced and delayed sleep phase syndrome can arise as well as transient chronobiologic disturbances, for example from jet lag and shift work.

Increasing evidence suggests that disrupted temporal organization of biological functions impairs behaviour, cognition, affect, and emotion. Furthermore, disruption of circadian clock genes impairs the sleep-wake cycle and social rhythms, which may be implicated in particular in mental disorders. An increasing number of journal publications point to a crucial role of circadian rhythm dysregulations in particular for affective disorders, which should e addressed specifically in modern psychiatry.

The seasonal variation of suicide corresponds to the annual fluctuation of some indices of central serotonergic metabolism indicating significantly lower brain serotonergic activity in spring and summer. Low central serotonin metabolism is a strong biological correlate of some pathological behaviours, like depression, impulsivity and violent suicidal acts.

Based on early findings suggesting that suicide seasonality might be the consequence of the seasonal incidence of depression-related suicides, we found that decreasing suicide seasonality might be a good marker of lowering rate of depressive suicides in the population. We recently analysed the relationship between increasing antidepressant utilization and national suicide rate of Hungary between 1998–2006, with particular regard to seasonal patterns and gender differences. Time trend analysis had been applied to investigate the correlation between trend of antidepressant prescription and both of suicide rates and seasonality index. During the 9 years of the study period there was a significant correlation between steadily increasing antidepressant prescription and continuous decline in total national suicide rate as well both in females and males, but this relationship was 8-fold stronger in males. Increasing antidepressant utilization was associated with significantly decreased seasonality of suicides only among males. As national suicide rates are affected by many factors the isolation of the result of better treatment of depression in declining suicide rates is not easy. Our results suggest that decreasing suicide seasonality could be a good marker of more widespread treatment of depression resulting in lowering rate of depression-related suicides in the population particularly among males.

The Circadian Locomotor Output Cycles Kaput (CLOCK) gene is thought to be involved in the regulation of circadian rhythms, with its protein products driving transcription of other genetic components of the molecular oscillator. The possible role of 3111T/C CLOCK gene polymorphism and a number of other variants in psychiatry is currently under investigation. A polymorphism in the 3’ flanking region of the CLOCK gene have been shown to affect mRNA stability and half-life, with possible significant effects on the level of protein finally being translated. In mice, a mutation of CLOCK gene, called “C” variant, has been shown to lead to a lengthened circadian period and in healthy humans the CLOCK*C allele has been investigated as a predictor of “eveningness.” Finally, a significantly higher recurrence rate of illness episodes has been found in bipolar patients homozygous for the C variant. In a series of studies, we investigated the possible effect of CLOCK variants in mood disorders and drug response.

Taken together, this evidence suggests that CLOCK gene variants modulate mood disorders in a subtle but consistent way, causing liability to a shorter and disrupted sleep, which is reflected in poorer sleep improvement during antidepressant therapy and eventually in a higher frequency of episodes. This also suggests the clinical usefulness of social rhythm therapy particularly in this subgroup of patients.

Aware of the huge and growing public health importance of depressive disorders the World Psychiatric Association developed an educational programme that brought together materials that psychiatrists could use in teaching other medical staff - for example general practitioners - about depression and its management. The programme was translated in many languages and widely used. Reports about the usefulness of the programme were very positive and usually drew attention to the fact that the programme contained a large amount of data that could be used in composing teaching curricula appropriate for the different settings in which the training was to take place. The experience gained in the use of the programme guided the development of the updated version of the programme released in 2009. As in the first edition, information was made available so that teachers could use in composing their educational activities. In addition however, a special chapter has been added to the programme addressing the role of culture in the presentation of depression and in its management. The presentation will describe the programme and its development. It will in particular describe the parts of the programme dealing with cultural issues and with the methods of education of general practitioners.

WHO has predicted that in 2020 depression will be the second most important cause of disability.

Studies focusing on cross- cultural aspects of depression have increased during the last decade, and depression has been studied cross-culturally regarding their prevalence and symptomatology.

The WHO study assessing depression across cultures reported a core symptomatology across the participating centres, but with certain differences in the ranking of problems in e.g. patients from non -industrialised nations somatic symptoms often dominate.

Furthermore, there is increasing focus on the impact of migration on depressive illness. Depressive syndromes are clearly very common in migrants, and are probably the most frequent mental disorders in people who move to other countries. Refugees and asylum seekers are subjected to significant social and psychological stress and are more vulnerable. For scientific purposes it is vital though to differentiate between the different aspects of influence, for example the frequency of disorders and problems in treatment. Results of studies on increased psychological morbidity in migrants do not indicate whether increased vulnerability is associated with a migration background, or with acculturation problems in the host country due to cultural differences, or a combination of both factors. Both culture and migration-specific factors, as well as the level of integration into the host country, determine the conflicting arguments.

The presentation will provide an overview of the burden of depression in relation to culture, differences in symptomatology, the role of migration and other circumstantial factors having an impact on the appearance and outcome of the disorder.

Intercultural psychotherapeutic treatment must involve the psychological integration of different cultures within an individual as an additional developmental dimension. The literature concerning acculturation and mental health yields heterogeneous results concerning strategies of adaptive acculturation. In intercultural psychotherapy the integration strategy is usually the strategy with the highest adaptability. It is still uncertain which theoretical assumptions might be applicable to a healthy acculturation process. However, it is assumed that increased acculturative stress may lead to higher risk and susceptibility for emotional distress and depression.

Individual change during the course of migration towards a bicultural identity that includes aspects of both the culture of origin and of the host culture has often been viewed as a desirable adaptation, although the theoretical foundation of the concept of bicultural identity remains inadequate. The cultural-dynamic model presented here distinguishes between personal and social identity on the basis of the identity concept proposed by Mead (1988). We discuss implications for the intercultural psychotherapeutic process, for identity configuration in second-generation migrants, for different phases of the lifespan, and in acquiring the language of the host culture.

A significant challenge in the culturally sensitive use of psychological and psychiatric instruments for depression is “bias”. Bias means that there is a lack of equivalence: Variation in the score is a result not of variation in the disorder or presence of the symptom in question but rather is due to “cultural factors”. Construct bias is perhaps the most complex of all, and is related to the very manner in which depression is understood. Psychological and psychiatric diagnostic and screening instruments delimit the very “nature” of depression, and fall prey to both false positives and false negatives when assessing individuals from cultures in which the experience and expression of depression is distinct from that found in the West. Equally complex are both method and item bias. In the former, the very method used—for example, a horizontal Likert-like scale—is responded to differentially across cultures, thus resulting in variance that is due not to variations in the presence of symptom but rather the manner of response. Item bias occurs when the item in question is understood in different ways in different cultures. Finally, there is concern about basic issues surround norms, cut-off scores and the like, in as much as the lack of equivalence indicates that results must be interpreted in accordance with population specific norms. Depression diagnostic and screening instruments and their items will be selectively reviewed to demonstrate the presence of bias, and concrete suggestions will be presented to achieve a more culturally sensitive assessment process.

The majority of the adults with ADHD have chronic difficulty to go to bed on time. This leads to a shorter sleep duration and daytime sleepiness that may aggravate the inattention problems of ADHD.

This sleep pattern is also known as a delayed sleepphase, and the patients as ‘eveningtypes’. The other way round, eveningtypes have been associated with impulsiveness. The scope of this presentation is to study the impact of this sleep pattern in adults with ADHD on mood (i.e. seasonal affective disorder), eating habits (like timing of meals and binge eating), activity patterns (like nightshift work and light at night) and health in general, i.e. obesity and cancer.

ADHD is a common neurodevelopmental disorder that persists into adulthood in around two-thirds of cases. Current operational definitions of ADHD focus on three core domains of inattention, overactivity and impulsivity, yet it is widely recognised that there is a wider range of psychopathology that co-occurs alongside these core symptoms. Among the most prevalent of these in adults with ADHD is mood instability, characterized by shifts in mood from ‘highs’ to ‘lows’, frustration, and chronic irritability. Mood instability may often be the main presenting symptom of ADHD and may also be one of the more impairing features of the disorder. Importantly, it has been noted that treatment for ADHD with stimulants or atomoxetine often results in improvements in mood instability symptoms in the same timescale as other core symptoms of ADHD, indicating that mood instability can be considered a symptom of ADHD just as much as inattention, impulsivity and hyperactivity. Here we report on key findings that show the very high correlation between ADHD and mood instability and the response of such symptoms to treatment with stimulant medications. Further work is aimed to clarify whether the problems with regulation of emotional responses and mood states seen in ADHD arise from the same underlying processes that lead to impaired regulation of attention and impulse control.

Pharmacological management for children and adolescents with ADHD should be part of a comprehensive treatment plan including psychological, behavioural, and educational advice and interventions. If pharmacological treatment is appropriate, stimulant medications and atomoxetine are the most effective medications for ADHD. The European ADHD Guidelines Group (a panel of ADHD experts from several European countries) has developed guidelines for the diagnosis and treatment of ADHD and published algorithms on the use of long-acting medications. Recently, the Guidelines Group has conducted a comprehensive review of the published literature on adverse effects of the drugs that are licensed in Europe, and most commonly used, for the treatment of ADHD or hyperkinetic disorder. This presentation will summarize those results and give an update on efficacy and safety issues concerning the pharmacological treatment of children and adolescents with ADHD.

The European Commission's Green Paper on Mental Health highlighted the need to improve the social inclusion, human rights and dignity, of mentally ill people. It recognised evidence for improved quality of life and social inclusion provided by deinstitutionalization of services. This study, funded by the EC, explores the relationship between unit characteristics and quality of care, as recorded by the Quality Indicator for Rehabilitative Care (QuIRC).

Metabolic syndrome, obesity, diabetes and other cardiovascular risk factors are highly prevalent in people with SMI. Patients are at risk for premature mortality and the mortality gap with the general population has increased over recent decades. In part these cardio-metabolic risk factors are attributable to unhealthy lifestyle, including poor diet, high rates of smoking, alcohol/substance use/abuse and sedentary behaviour. But over recent years it has become apparent that antipsychotic agents and other psychotropic agents can have a negative impact on some of the modifiable risk factors. Also other somatic co-morbid disorders are also linked to antipsychotic treatment such as the consequences of hyperprolactinaemia, QTc-prolongation and constipation. Other somatic disorders such as poor dental care, HIV and other infectious diseases and some forms of cancer are also more prevalent in patients with schizophrenia. People with SMI also have limited access to effective screening and somatic care. The psychiatrist needs to be aware of the potential somatic side-effects of antipsychotic medication and to include them in the risk/benefit assessment when choosing a specific antipsychotic. He should also be responsible for the implementation of the necessary screening assessments and referral for treatment of any physical illness. Multidisciplinary assessment of psychiatric and medical conditions is needed. The somatic treatments offered to people with severe and enduring mental illness should be at par with general health care in the non-psychiatrically ill population.