Psychiatry deals with morbid psychological experience. This suggests that central to psychiatry's concern is the mind as opposed to the body. Yet, it is often the afflicted body rather than the mind that the patient presents to the clinician. In addiction, psychiatry classification has an underlying hierarchical bias for organic (somatic) disorders. Furthermore, many disorders such as generalised anxiety disorder and mood disorders have bodily manisfestations that are taken for granted in the consultation process or translated and relabelled as pointing towards psychological/emotional distress. This suggests that Cartesian mind-body dualism continues to significantly influence psychiatric concepts, classification and practice. In this presentation, the role of the body as model, metaphor, symbol, object and experiencing subject will be analysed with illustrative examples from clinical practice and literature. I will rely on Kafka's Letter to Father, Elfriede Jelinek's Piano Teacher, and Minkowsky's Lived Time.

The psy fields are predicated on the cartesian notion of a mind-body dualism.Suffering is understood to stem either from problems of mind or from problems ofphysiology. A related dualism is that of the “biological” and thatof “cultural”. Recent commentators have worked at great length tocollapse this dualism in day to day work with patients. At the same time, itclearly forms a fundamental part of medical epistemology. From a transculturalperspective, it is increasingly clear that there exists the possibility forconsiderable difference in the four “Es”: Experience, expression,explanation and expectations related to suffering. This variation is in largepart related to the epistemic structure underlying any given culture, and, takenas such, can present a considerable challenge to consultation-liason psychiatry.A patient may experience suffering that is expressed in the form of strangesensations in a specific parts of the body. This is then explained as aconsequence of a certain process that is culturally syntonic, and then expects acertain course of suffering as well as treatment. Given that we tend to take ourepistemic perspectives for granted as representative of the “world as itis”. The C-L psychiatrist who does not take these variations intoconsideration could all to easily arrive at a misdiagnosis and as sucherroeneous treatment.

Somatization concept should be considered in biopsychosocial integrity. Thispresentation reviews the social aspects of somatization. The description ofsomatization evolved in time in order to include the social aspects. Thedifferences of somatization between societies, somatization concept in westernand Eastern medical thought, modernist theory on the evolution of somatization,research which confirm and which do not confirm the modernist theory werereviewed. The pos-modern approach which constitutes a new paradigm in culturalpsychiatry, prefers to study the mental disorders through the culture, insteadof comparing them cross-culturally. In this context, first the culture-boundsomatization diagnosis of non-Western cultures, then the fashionable diagnosisof Western culture in which the somatization is hiding were reviewed.

ADHD is often associated with symptoms of emotional lability (EL), such as irritability, hot temper, low frustration tolerance, and sudden unpredictable shifts towards negative emotions such as anger, dysphoria and sadness. EL has been consistently noted in the changing definitions of the ADHD construct and its diagnosis and is currently considered an associated feature of the disorder. However, it is still unclear how EL and ADHD are interconnected. Thus, 1186 children with ADHD-combined type and 1827 siblings (aged 6-18 years) were assessed for symptoms of EL, ADHD, associated psychopathology and comorbid psychiatric disorders with a structured diagnostic interview as well as parent and teacher ratings of psychopathology. EL was associated with increased severity of ADHD core symptoms, particularly hyperactivity-impulsivity, and more symptoms of comorbid psychopathology, primarily symptoms of oppositional defiant disorder (ODD), but also affective symptoms, and substance abuse. However, EL was only partly explainable by the severity of ADHD core symptoms and associated psychopathology, and seems to be more closely related to oppositional symptoms. Severity of EL in probands increased severity of EL in siblings but not prevalence rates of ADHD or ODD.

The dimensions of ADHD symptoms in adults have been discussed controversially. Beside the classical symptom domains as unattention, hyperactivity, and impulsivity, other symptom clusters as emotional dysregulation are in debate. The aim of this presentation is to update the recent discussions on this topic by reviewing current positions and empirical data as well as presenting own data. The relationship between the scales with emotional contents in the Wender-Reimherr Adult Attention Deficit Disorder Scale (WRAADDS) compared to other established ADHD rating scales was explored in a sample of 600 ADHD patients. The aim is to clarify whether the symptoms are independent of other ADHD domains.

ADHD in adults is frequently associated with unstable or irritable moods reflecting difficulties with emotion regulation. Effect sizes of drug treatments on symptoms that reflect difficulties with emotion regulation, are similar to those on core ADHD symptoms, with co-variation of around 0.8 between the two types of symptoms during the treatment response. We therefore set out to investigate whether variability in mood results from the same aetiological processes that lead to variability in behaviour and cognitive performance in ADHD. Using real-time self-monitoring of emotional states and ADHD symptoms every two hours for 3-5 days, we characterised the mood changes in ADHD. Variability in both mood and ADHD symptoms (measured as the standard deviation) were significantly correlated with self-rated ADHD symptoms of inattention and hyperactivity. Subsequent analyses will link the observed symptom changes to cognitive-electrophysiological measures which are reliable indicators of core processes that underlie cognitive deficits associated with ADHD. We previously showed that a familial reaction time (mean and variability) factor explains 70% and commission and omission errors 20%, of the familial effects on ADHD. This finding concurs with the developmental model of Halperin which postulates that ADHD is linked to an early-appearing and enduring subcortical dysfunction, reflected in reaction time variability, while persistence/desistence of ADHD is dependent on maturational changes in executive control during adolescence reflected in commission and omission errors. We propose that at a behavioural level the subcortical deficit leads to dysregulation of a number of processes, including attentional, impulsive and emotional control.

The core psychopathology of ADHD comprises attentional deficits, hyperactivity and impulsivity. At least in subpopulations the majority of individuals suffering from ADHD present with emotional symptoms additonally. There is an ongoing and controversial debatte whether emotional symptoms belong to the disorder as further intrinsic ADHD psychopathology or may have their origin in comorbid affective disorders. There is growing evidence that emotional symptoms of ADHD as measured by the Wender-Reimherr Adult Attention Deficit Disorder Scale (WRAADDS) respond to treatment with Methylphenidate (MPH), while the classical symptoms of depression or anxiety disorder show no significant improvement.

We report on a 24-week, placebo controlled treatment study with MPH-extended release in 359 adults with ADHD. Emotional symptoms were assessed with the WRAADDS. Symptoms of depression and anxiety were endorsed by use of the Symptom Checklist-90-Revised (SCL-90-R).

As compared with placebo we found a significant treatment response in favour of MPH-ER regarding emotional symptoms like affective lability, emotional overreactivity and temper control. The psychopathology of depression and anxiety did not display a significant treatment response.

There is strong evidence for a heritability of major depression as shown by family, twin- and adoption studies. Several studies suggest a heritability for unipolar depression between 35 and 75% which is much lower than the heritability of bipolar disorder or schizophrenia. There is no doubt, that major depression is not caused by any single gene but it is a disease with complex genetic features. Furthermore, some subtypes, as early-onset or recurrent depression may have a higher heritability than other forms of depression. Neuroticism as an intermediate phenotype of MDD, which is a trait that reflects a tendency toward negative mood states, and has been linked to internalizing depressive conditions. For these reasons Dan Rujescu will present genome-wide and candidate gene studies, demonstrating a genetic approach for discovering potentially important pathogenic pathways for which clinically powerful (bio)markers may eventually be developed. He will discuss neuroticism as an intermediate phenotype of MDD, which is a trait that reflects a tendency toward negative mood states and has been linked to internalizing depressive conditions.

cAMP-specific PDE4 are a family of enzymes capable of hydrolyzing cAMP to 5’AMP. cAMP plays a major role in synaptic plasticity, neurite outgrowth, and neuronal differentiation and survival and recent studies demonstrate involvement of cAMP in pathophysiology of depression. The cAMP-specific PDE4 can be differentiated from other PDE families by sequence identity in the catalytic region of the protein and by their ability to be inhibited by a specific class of drugs, of which rolipram is the prototype. PDE4 enzymes are also unique in having ‘signature’ regions of sequence, called upstream conserved regions (UCR1 and UCR2), located in the N-terminal region of the proteins. There are four PDE4 subfamilies, encoded by separate genes (PDE4A, PDE4B, PDE4C, PDE4D), all are expressed in brain. A few studies suggest that PDE inhibitors show antidepressant-like effects in rodents. To examine the role of PDE4 in depression, we characterized various isoforms of PDE4 in human brain. Expression of PDE4A1, PDE4A4, PDE4A10, PDE4B1, PDE4B2, PDE4B3, PDE4D3, PDE4D4, PDE4D5 and PDE4D9 variants were characterized. All, except PDE4A10, PDE4B1, PDE4D4 or PDE4D5 variants, were highly expressed in human brain. When compared, we found that expression levels of PDE4A1, DE4B2, and PDE4A4 were decreased in PFC and hippocampus of depressed subjects, whereas, no change was observed in expression of PDEB3, PDE4D9, and PDED3 variants. Our study for the first time provides evidence of variant specific alterations in PDE4 in brain of depressed subjects and indicates that these variants may be used as site-specific therapeutic target(s) to develop novel antidepressants.

The aim of the “Therapy Evaluation Project” was to examine the therapy outcomes of all violent and sex offenders treated by the Zurich Criminal Justice System between January 1997 and the 31st of December 2005.

This included all the court-ordered therapies at the prisons of the Canton of Zurich as well as outpatient treatments that were carried out after release from detention (or instead of detention). The final treatment sample consisted of N=222 treated violent and sex-offenders. A representative sample of untreated violent and sex-offenders served as a control group.

After a mean time at risk of six years, the recidivism rates of the offenders were reviewed. Two types of recidivism were defined:

1. (1) The listing of a new conviction in the criminal record or

2. (2) offense relevant behaviour documented by the therapists, the probation services and/or other authorities.

The recidivism rate for treated violent and sex-offender was 12% compared to 20% for the untreated controls. By juxtaposing the various criteria/definitions of recidivism, the standards for evaluating the effectiveness of therapy will be debated.

The topic of this symposium is the evaluation of outcomes in individuals presenting with violent or sexual offending in a range of different settings. Violent offenders are of particular concern to psychiatrists who may face pressure from society to detain such individuals. At the same time evidence for the efficacy of any interventions to improve outcome and reduce re-offending remains limited. In recent years new initiatives (e.g. the programme for Dangerous and Severe Personality Disorders (DSPD) in the UK) have been developed to understand better what works for violent offenders, including those with personality disorders. Research in this area is complex not least as randomised controlled trials might not be seen as practical or ethical.

This symposium comprises speakers from three different countries, Sweden, Switzerland and UK. The Swedish contribution will present data from a naturalistic study comparing offenders with mental disorder and substance misuse who engage in community treatment following release to those who don’t. Researchers from Switzerland will introduce the “therapy evaluation project” of the Zurich Criminal Justice System and show data on recidivism (both convicted and non-convicted). Presenters from the UK are from one of the high secure DSPD sites and will present different methodologies, including single case studies, to evaluate the efficacy of this service and its different therapies. The implications of these findings for future research and service delivery will be discussed.

Suicidal behavior (SB) is a major burden in most nations world-wide and a major public health concern. The causes of SB are complex, in which both genetic set-up and exposure to overwhelming psychological stress (environmental factor) contribute to a person's final predisposition for SB. One candidate system reflecting this causal route to SB is the stress-modulating hypothalamic-pituitary-adrenal (HPA) axis, and dysregulation of HPA is considered to play a major role in depression and SB. The corticotrophin-releasing hormone and its main receptor (CRHR1) have key regulatory functions in the HPA axis, and we hypothesized that genetic variation in CRHR1 may be associated and linked with SB and related endophenotypes. We analyzed single nucleotide polymorphisms (SNPs) in an extended sample of family trios (n = 672) with suicide attempter offspring, by using family-based association tests. Results showed that the minor T-allele of exonic SNP rs12936511 was significantly transmitted to suicidal males with increased Beck Depression Inventory (BDI) scores (P = 0.0028). Analysis of haplotypes showed that risk alleles of three different SNPs segregated onto separate haplotypes, whereas a fourth ‘nonrisk’ haplotype (‘CGC’) was preferentially transmitted to suicidal males with lowered BDI scores (P = 0.0007). Conversely, the BDI scores of those who carried a homozygous combination of any of the three risk haplotypes were significantly increased (P = 0.000089). We concluded that depression intensity in male suicidal offspring was related to genetic variability in the 5’-end of CRHR1, while the characteristics of the suicide female attempters remained unknown.

Suicide is the leading cause of death in prisons. Number of studies has indicated disturbances in serotonin neurotransmission in persons displaying suicide behaviour and depression. We hypothesized that 5-HT2A -1438G/A polymorphism would modulate the influence of childhood trauma on suicide and depression among prisoners in a gene-environment-dependent manner.

Study participants were 427 male prisoners detained in jails of the District of Abruzzo-Molise in Italy. All were assessed through psychiatric interview, Hamilton Rating Scale for Depression (HRSD-21 items) and Childhood Trauma Questionnaire (CTQ). The component structure of the 21 HRSD items was determined using principal component analysis with varimax rotation and three components were extracted. We proposed a new gxe model with all components dichotomised at the median and used as dependent variables when creating logistic regression.

Significant interactions were found with the suicide/insomnia component only. The major findings were:

1. 1) emotional abuse during childhood interacts with 5-HT2A AA genotype to increase the risk for later-life suicide and insomnia,

2. 2) 5-HT2A AA genotype and childhood traumas (emotional abuse and physical neglect) independently of each other increased the risk for later-life suicide and insomnia,

3. 3) 5-HT2A AG and GG genotypes might be protective against suicide and insomnia, even when in interaction with childhood traumas.

Our results add evidence to the fact that suicide and insomnia are both complex traits shaped by interactions between genetic and environmental factors. These factors might interact dynamically throughout prenatal and postnatal periods, thus shaping the brain development and leaving long-term consequences on adult behaviour.

In the Netherlands, the Depression Initiative has been launched in 2006 as a nationwide attempt to implement the Multidisciplinary Guideline for Depression and to evaluate its cost effectiveness. An evaluation of the selected strategy to implement the guidelines, a Breakthrough Collaborative, was conducted as a quasi experimental trial. The intervention group consisted of around 530 patients coming from 10 multidisciplinary teams in primary care. The intervention teams received a set of implementation strategies, as part of the Breakthrough Method, developed by the Institute for Healthcare Improvement (www.ihi.org). The aim of the participants in this implementation project was to implement guideline recommendations directed at a reduction of unnecessary antidepressant treatment for patients with mild depression, better use of effective, but minimally invasive treatment options and improved antidepressant and psychotherapeutic treatment for patients with severe symptoms. Monitoring depression severeness was also one of the goals. This guideline derived, stepped care approach was compared to Care As Usual in the primary care setting, as provided in a different study group (NESDA). Outcomes were measured in terms of quality of care provided by the general practitioner (antidepressant prescription rates) and clinical outcomes (BDI, IDS-SR, WHODAS). A process evaluation and simple economic evaluation was part of the study design. In the presentation, preliminary results will be presented.

In the Netherlands, the Depression Initiative has been launched in 2006 as a nationwide attempt to implement the Multidisciplinary Guideline for Depression and to evaluate its cost effectiveness. Evaluation of a collaborative stepped care model in several health care settings is one of the objectives of the Depression Initiative. Currently a stepped collaborative care project is being evaluated in the primary care setting, evaluating stepped collaborative care for depressive disorder provided by the primary care practitioner, a nurse-care-manager, and a consultant psychiatrist, in a Randomised Controlled Trial. 150 Patients with depressive disorder are offered a treatment plan. They can choose from two options: Problem Solving Treatment with or without antidepressant treatment. The medication is prescribed by the PCP, PST and monitoring is provided by the care manager, and the psychiatrist can be consulted every 6 weeks in order to see if the intervention is sufficient to improve the symptoms of the patient. The PHQ is used for monitoring. A two step approach is aimed at; if the patient does not achieve remission after 18 weeks, the patient is referred to mental health care. This stepwise approach is supported by a training and supervision program and by a web-based tracking system in which the care-manager and the patient can monitor progress and consult the psychiatrist. This approach is compared with Care As Usual in the primary care setting. In the presentation, preliminary results will be presented.