Minor motor and sensory deficits or neurological soft signs (NSS) are frequently found in individuals suffering from schizophrenia at any stage of their illness. The basal ganglia and the thalamus are accepted as being important for both motor control and integration of sensory input. However, whether NSS are related to structural alterations of these brain regions remains controversial.

20 patients with a first-episode psychosis were investigated using high-resolution magnetic resonance imaging (MRI) at 3 Tesla. NSS were examined on the Heidelberg Scale after remission of acute symptoms and correlated with volume and shape of striatum, pallidum and thalamus by using sophisticated MRI analyses, namely VBM-DARTEL (volume) and FSL-FIRST (shape).

Results NSS scores in patients with schizophrenia were significantly associated with volumetric changes and surface alterations in all investigated areas. Associations remained significant when controlling for age, gender, education, medication and intracranial volume.

Our findings lend further support for an involvement of the basal ganglia and the thalamus in NSS.

Experience-dependent cortical plasticity observed during post-training sleep has been hypothesized to be part of the global process of memory consolidation. Combining the temporal resolution of microstructure detectors and the spatial resolution of low-resolution brain electromagnetic tomography (LORETA) makes it possible to investigate when and where the experience-dependent reactivation occurs under normal (undisturbed) sleeping conditions.

After an adaptation night, in the 2nd and 3rd night 48 young healthy volunteers were randomly assigned either to a control condition or to an experimental condition (declarative memory task: paired-associate word list or procedural memory task: mirror tracing). Sleep stages and sleep microstructures (slow waves, spindles and theta bursts) were detected automatically by means of the Somnolyzer 24x7. Changes in LORETA sources (experimental minus control night) were correlated with changes in memory performance (morning minus evening recall).

Overnight improvements in the mirror tracing task were correlated with increased slow-wave sources in the right posterior parietal cortex (r = .70,p < 0.01) during NREM sleep and with desynchronized (r = −.76,p < 0.01) and synchronized (r = .62,p < 0.01) rolandic mu rhythm sources during periods with theta bursts in REM sleep. Overnight improvements in the declarative memory task were significantly correlated with increased spindle sources (r = .52, p < .01) in frontal, temporal and cingulate brain regions.

The present study supports the hypotheses of (1) a use-dependent reset of synaptic plasticity during slow-wave sleep (restorative function), (2) an experience-dependent reactivation during spindle episodes (stabilizing function) and (3) an off-line neuronal reprocessing during REM sleep (improvement without further training for novel tasks).

Alcohol-induced psychotic disorder (AIPD), is an uncommon complication of alcohol abuse. AIPD needs to be distinguished from alcohol withdrawal delirium and schizophrenia and the underlying pathophysiology is poorly understood. Few brain-imaging studies in AIPD have been reported to date. Case reports of brain-imaging in AIPD suggest possible dysfunction in the thalamus, basal ganglia, frontal lobes and cerebellum. The aim of this study was to compare resting brain perfusion (rCBF) in patients with AIPD, uncomplicated alcohol dependence, schizophrenia and healthy volunteers.

Single photon emission computed tomography (SPECT) was utilized to compare rCBF in patients with AIPD (n = 19), schizophrenia (n = 16), uncomplicated alcohol dependence (n = 20) and healthy volunteers (n = 19).

Increased rCBF was demonstrated in the right calcarine area in patients with AIPD compared to healthy volunteers, with a trend towards increased rCBF to the frontal and temporal lobes and the right pallidum. Decreased left sided rCBF to the putamen, parietal, mid-frontal and mid-temporal lobes and heterogenous flow to the cerebellum were demonstrated in patients with AIPD when compared to patients with uncomplicated alcohol dependence. The left posterior cingulate and right cerebellum showed higher and lower rCBF respectively in patients with AIPD compared to patients with schizophrenia.

The findings implicate the right occipital lobe and possibly the cerebellum in the pathogenesis of AIPD. Some findings have similarities with rCBF reports in alcohol-withdrawal. Reduced rCBF to the frontal lobes, thalamus and basal ganglia in AIPD as suggested in previous case reports could not be confirmed.

Citalopram is a widely applied SSRI in patients suffering from affective disorder. It is a racemic mixture of the S- and R-enantiomer of citalopram, consisting of equal parts of S-citalopram and R-citalopram, respectively. It has been shown that the inhibitory potency in serotonin reuptake of S-citalopram is much higher compared to R-citalopram, and it is assumed that S-citalopram is the main carrier of the antidepressant effect.

Here we investigated the effects of the two SSRIs Citalopram (50% S-, 50% R-citalopram) and Escitalopram (100% S-citalopram) on brain networks during emotion processing using pharmacological functional magnetic resonance imaging (fMRI) and dynamic causal modelling (DCM), an advanced tool to investigate functional integration between different brain regions.

Our results are based on a placebo-controlled, randomized, double-blind, cross-over pharmacological study in 16 healthy subjects during three fMRI scanning sessions performing a facial emotional discrimination paradigm (Windischberger, Neuroimage, 2010). 32 models of pharmacological modulation within the amygdalar-parahippocampal-orbitofrontal network were analysed using Bayesian Model Averaging (BMA) as implemented in SPM8.

S-citalopram showed statistically significant modulatory effects on forward amygdala-orbitofrontal and bidirectional amygdala-parahippocampal connections. No significant modulatory effects of R-citalopram were found.

This is the first fMRI study that showed stimulus-specific differential effects of the two enantiomeres R- and S-citalopram at the neural connectivity level. Our results corroborate studies in rats where escitalopram-induced increases in extracellular serotonin levels were found attenuated when R-citalopram was coinjected. Taken together this might explain the response differences between study drugs as demonstrated in previous clinical trials.

There are indications that psychiatric patients do not receive adequate treatment of their somatic diseases.

To evaluate the effect of mental disorder on the risk of mortality.

To study whether severity of psychiatric disease increases the risk of mortality.

A register-based cohort study comprising all individuals alive and registered in Sweden in 2004 and 2005 aged 20–64. We followed 5,181,743 individuals with respect to mortality 2006 and 2007, generating 10,261,263 person-years and 24,475 deaths. Psychiatric patients were defined as those treated with a main diagnosis of psychiatric disease within the last five years and were classified according to type of mental disorder: psychoses, depression/anxiety, substance abuse, and other psychiatric diagnoses. We studied all cause mortality, mortality from ischemic heart disease, suicide, violent deaths, smoking related cancer and policy-related and health care-related avoidable mortality. Estimates of risk of mortality were calculated as incidence rate ratio (IRR) with 95% confidence intervals (CI) using Poisson Regression Analysis.

Patients with schizophrenia or other psychosis in general had the highest mortality for most mortality outcomes. For both women and men, those treated for substance abuse had the highest all-cause mortality risk (Women: IRR = 12.56 (95% CI = 10.82–14.57); Men: IRR = 9.38 (95% C = 8.73–10.08). For all psychiatric diseases and for all mortality outcomes those on social benefits had a higher mortality.

Psychiatric patients have a higher overall mortality and cause-specific mortality. The more severe the psychiatric disease the higher is the risk of mortality even after disregarding violent deaths and suicide.

There are concerns that people with mental disorders may not receive proper somatic care within health care systems, and face the risk of poor physical health outcomes and premature death.

To study whether patients with diabetes and comorbid mental illness are at higher risk of amputation of the lower limbs and mortality than diabetic patients without mental illness.

To pinpoint possible disparities in physical health outcomes and mortality in diabetic patients with or without mental disorders.

National Swedish registers; Prescribed Drug Register, Patient Register and Cause of Death Register. All subjects that were prescribed antidiabetics during 2006, at age 35–79, were included (n = 229,956). Subjects with at least 2 hospital inpatient stays during 1996–2005 for psychotic disorders, i.e. schizophrenia/affective psychosis (n = 2,791), or non-psychotic disorders, i.e. depression/anxiety (n = 2,327) were identified. The study population was followed from 2007–2009. A Poisson regression model estimated the effect of mental illness on the likelihood of amputation or death. Incidence rate ratios (IRR) and 95% confidence intervals (CI) were calculated.

Diabetic patients with comorbid psychotic and non-psychotic illness were more likely to die than patients without mental illness, also when suicides and events of undetermined intent were excluded (IRR = 2.44, CI 2.18–2.72 and IRR = 2.43, CI 2.17–2.71, respectively). The risk of amputation was particularly enhanced in diabetic patients with depression or anxiety (IRR = 4.39, CI 2.58-7.49).

In diabetic patients there exist unsettling disparities in physical health outcomes and mortality that are associated with whether a person is mentally ill or not.

Prospective data on depressive symptoms and blood pressure (BP) are scarce, and the impact of age on this association is poorly understood.

The present study examines longitudinal trajectories of depressive episodes and the probability of hypertension associated with these trajectories over time.

Participants were 6,889 men and 3,413 women London based civil servants followed for 24 years between 1985 and 2009. The age of participants over the follow-up ranged from 35 to 80 years. Depressive episode (defined as scoring 4 or more on the General Health Questionnaire-Depression subscale or using prescribed antidepressant medication) and hypertension (systolic/diastolic blood pressure ≥ 140/90 mm Hg or use of antihypertensive medication) were assessed concurrently at five medical examinations.

In longitudinal logistic regression analyses based on Generalized-Estimating-Equation using age as the time scale, participants with depression trajectory characterised by increasing depressive episodes overtime had a greater increase in the likelihood for hypertension with advancing age; an adjusted-excess increase of 7% (95% CI 3-12, p < 0.001) for each five-year increase in age compared to those with a low/stable depression trajectory. In a model adjusted for relevant confounders, a higher risk of hypertension in the first group of participants did not become evident before age 55. A similar pattern of association was observed in men and women although the association was stronger in men.

This study suggests that the risk of hypertension increases with repeated experience of depressive episodes over time and materializes in later adulthood.

The consequences of work-related violence and threats for clinically significant mental health problems are unclear: One study showed associations with hospitalisation for depressive and stress-related disorders, but a different study found no association with use of antidepressants. This null-finding, however, could be due to lack of statistical power.

Re-examining the relation between exposure to work-related threats and violence in a large sample of Danish employees (n = 15527).

Assessing whether employees reporting exposure to work-related threats or violence are more likely to start treatment with psychotropics.

We synthesized three Danish studies with self-reported data on exposure to work-related threats or violence within the past 12 months and linked it with purchases of psychotropic medications through registry-data. After excluding 1750 respondents who had used psychotropic medication previous to 12 months before questionnaire-response, the final study population was 15527 employees. We examined four mutually exclusive outcomes:

1. 1) antidepressants (N06a),

2. 2) anxiolytics (N05b),

3. 3) antidepressants and anxiolytics,

4. 4) hypnotics only (N05c).

Using four separate logistic regressions we adjusted risk estimates for confounding by gender, age, cohabitation, education, and income.

Preliminary analyses show increased risk for treatment with antidepressants (OR = 1.46; 95%CI: 1.15–1.86) and antidepressants combined with anxiolytics (OR = 1.79; 95%CI:1.16–2.76), but not anxiolytics (OR = 1.04; 95%CI: 0.74-1.45) or hypnotics only (OR = 1.08; 95%CI: 0.77–1.50). Final results will be available for the conference.

In this large sample of Danish employees, exposure to threats or violence in the workplace is associated with treatment with antidepressants, and antidepressants combined with anxiolytics, but not anxiolytics or hypnotics only.

It is not well known whether the association between common mental disorders and low socioeconomic status vary with symptom severity, type of socioeconomic indicator or gender.

To study the association between socioeconomic status and risk for different severity levels of psychological distress as well as depression.

A population-based survey was conducted among a random sample of Stockholm County residents aged 18–84 years in 2002, and respondents were reassessed via a follow-up questionnaire in 2007. Participants in both surveys (n = 23 794) were categorized according to socioeconomic status at baseline and followed up for onset of psychological distress (according to the twelve-item general health questionnaire) and depression (according to health data registers).

Occupational class had little impact on risk for distress regardless of severity or gender, but was strongly associated with onset of depression - albeit only in men (ORs being 3.0 [95% CI 1.5–5.9] in men and 1.1 [95% CI (0.7–1.7]) in women, comparing unskilled manual workers with higher non-manual workers). Income was associated with risk for onset of all outcomes and the association grew stronger with symptom severity. High household income was particularly protective of depression in women. Education was unrelated to either outcome in men and women overall.

While psychological distress appears to occur at a similar rate regardless of socioeconomic position, risks for severe distress and especially clinically overt depression are markedly linked with occupational class in men and with family income in women. The socioeconomic gradient in common mental disorders increases with symptom severity.

The chronic worldwide shortage of psychiatrists has impaired the delivery of first class mental health care. The WHO produced a report on the Mental Health Gap, showing the high burden of mental health, neurological and substance misuse disorders worldwide, estimating a treatment gap of 75% between need and resources.

Research to date has highlighted key areas that influence students' choice of a career in psychiatry. There have been several key literature reviews summarising work in the area since the 1950s. The current study updates literature with a systematic review of the past 10 years.

A five level search strategy was used.

A standard Critical Appraisal tool was developed based on the one used by the Best Evidence in Medical Education Group in Dundee. Papers were coded and graded using hierarchies of evidence - Sackett Hierarchy of Evidence and Kirkpatrick Hierarchy.

The quality of published studies has risen over the past 30 years, with the past decade producing the most robust evidence. However, it is a complex area to research with many potential confounders, and large gaps in knowledge remain.

Attention plays an important rol in pain perception. Focusing attention in pain intensifies the painful experience whereas distraction may decrease its subjective sensation (Eccleston & Crombez, 1999).The purpose of the two studies is to establish the efficacy of distraction by means of VR in the control and reduction of pain using the cold-pressor test. In both studies threshold, tolerance, perceived pain intensity and time estimation were measured.

37 healthy participants were induced pain in two consecutive immersions using the cold-pressor test. The experiment was counterbalanced and all participants went through two experimental conditions: VR (stereoscopic screen) and black screen. A virtual environment “Surreal World” was designed based on distraction of attention techniques. Results showed that VR significantly increased threshold and tolerance, diminished pain intensity and perception of time.

35 healthy participants underwent two consecutive immersions using cold pressor: VR (using the updated version of Surreal World and 3D laptops) and black screen. VR significantly increased the threshold and tolerance, whereas variations in the estimation of time were barely significant.

Differences in the results of the two studies could be accounted for by the immersive effect of the stereoscopic screen. Findings are discussed in relation to previous studies on VR and pain. Results support VR as an adjunctive method in pain treatment and allow proving its efficacy in patients with chronic pain.

There is a high co-morbidity between chronic inflammatory disorders and depression1. Proinflammatory cytokines like TNFα seems to play a central role in the pathogenesis of these disorders and its neutralization provides a potent treatment for inflammatory disorders2. Trying et al (2006) showed that a TNF-α blocker -etanercept- caused at least a 50% improvement in depression scores in psoriasis patients.3 These observations together with the theoretical background led to the hypothesis that TNF-α blockers may reverse depressive symptoms associated with chronic inflammatory disorders.

To evaluate the effectiveness of TNF-α blockers on symptoms of ankylosing spondylitis (AS) and depression.

9 treatment resistant AS patients with no contraindications for TNFα blockers, who were not using any psychotropic or nonbiological drugs were enrolled for the study. TNF-α blockers were given at weeks 0, 2 and 6 and Hamilton Depression and Anxiety Scales (HAMD, HAMA), Hospital Depression and Anxiety Questionnaire (HAD), Quality of Life Scale (SF36), AS severity index (BASDAI) was applied to the patients at week 0, 2 and 6.

There was a significant reduction in HAMD (p = 0.00), HAMA (p = 0.00), HAD-anxiety scores (p = .004) and a significant improvement in SF36- physical role (p = 0.00), physical role limitations (p = 0.01), bodily pain (p = 0.01), general health perception (p = 0.00), vitality (p = 0.02) and emotional role limitations (p = 0.01) subscales and BASDAI scores (p = 0.00) from week 0 to weeks 2 and 6.

This study showed that TNFα blockers may have a potential antidepressant effect besides its antiinflammatory effect in AS patients in a small sample.

To investigate the relationship between adaptive, maladaptive, and pathological Internet use and mental health problems, in particular depression, self-harm and suicidal behavior among a representative sample of adolescents from different European countries.

A total of 7.000 students from different European countries were recruited for the SEYLE study, a European school-based intervention study, and completed a self-report questionnaire for baseline assessment. Internet behaviors were evaluated by the Young Diagnostic Questionnaire, depression by the BDI-II, self-harm by the Deliberate Self-Harm Inventory and suicidal behavior by the Paykel Suicide Scale.

Pathological Internet users, who met the criteria for Internet addiction, showed significantly higher rates of depression, self-harm and suicidal behavior compared to students with adaptive Internet use. Remarkably, there were no significant differences in depression as well as self-harm and suicidal behavior between students suffering from Internet addiction and students presenting maladaptive Internet behaviors.

These results clearly demonstrate that students presenting either Internet addiction as well as maladaptive Internet use are more likely to suffer from depression as well as self-harm and suicidal behaviour. However, the group of students with Internet addiction and the students presenting maladaptive Internet use did not significantly differ from each other. These results suggest that not only Internet addiction, but also maladaptive Internet use, is associated with symptoms of depression, self-harm and suicidal behavior. Therefore, more attention should be paid to adolescents with maladaptive Internet use in order to early recognize depression, self-harm and suicidality in adolescence.

Depression is the most frequent psychiatric disorder. Antidepressant drug treatment response is modulated by genetic factors. Tianeptine molecule does not inhibit serotonin reuptake. Possible targets to this treatment are the serotonin transporter (5HTT/SLC6A4), the serotonin receptor 2A (5HT2A) and, the neuronal-specific enzyme that controls brain serotonin synthesis, the tryptophan hydroxylase-2 (TPH2).

We screened variants of candidate genes 5HTT/SLC6A4, 5HTR2A and THP2 in 3500 outpatients treated with tianeptine for a major depressive episode (MDE) to search for an association to a positive treatment response.

The goal of this work was to study the pharmacogenetic response to tianeptine treatment in MDE.

A total of 3500 outpatients were treated with tianeptine for a MDE. The criteria for a MDE were examined by the clinicians according to the DSM-IV diagnosis and the duration of each symptom was recorded during the inclusion and at 4 to 8 weeks of treatment. The Hospital Anxiety and Depression Scale (HAD) was evaluated at the two visits. DNA was extract from saliva sample and genotyping of single nucleotide polymorphisms (SNPs) was performed by Taqman assay.

All clinical and genotype data were collected for 1855 tianeptine-treated patients. The SNP rs6354 in SLC6A4 gene was significantly associated with response to tianeptine (p = 0.009; Odds ratio = 1.26; 95% confident interval = 1.06–1.50). Two SNPs in 5HT2A and one in TPH2 were also associated to treatment response (rs7322347 p = 0.03, rs7997012 p = 0.04 and rs7955501 p = 0.04).

We detected a pharmacogenetic association between serotonin genes and the response to tianeptine in major depressive episode.

Ghrelin showed antidepressant-like effects in mice. Furthermore, ghrelin influences sleep and the activity of hypothalamic-pituitary-adrenal (HPA) and somatotropic axis in healthy humans as indicated by increased cortisol and growth hormone (GH) plasma levels. Both sleep and the activity of these endocrine axes are disturbed in depression.

To study the effect of ghrelin on psychopathology, sleep and secretion of cortisol and GH in patients with major depression.

Depressive symptoms as assessed by a validated self rating scale (’Befindlichkeits-Skala’, [well-being scale]), secretion profiles of cortisol and GH and sleep-EEGs were determined in 14 unmedicated patients with major depression (7 women) twice, receiving 50 μg ghrelin or placebo at 2200, 2300, 0000, and 0100 hours.

Overall, depressive symptoms did not change significantly after ghrelin administration (placebo: 37 ± 8; ghrelin: 33 ± 10, p = 0.178). However, there was an improvement at trend level in men (placebo: 36 ± 9 to ghrelin: 30 ± 9, p = 0.093) but not in women. In men, ghrelin was associated with less time awake (placebo: 149.0 ± 11.1; ghrelin: 88.0±12.2 min, p = 0.029) and more non-REM sleep (placebo: 263.2 ± 24.1; ghrelin: 304.9 ± 14.1 min, p = 0.027), in women with less REM sleep (placebo: 108.6 ± 15.7; ghrelin: 74.1 ± 13.8 min, p = 0.031) and longer REM latency (placebo: 49.9 ± 6.5; ghrelin: 85.6 ± 14.1 min, p = 0.019). In both sexes, ghrelin caused strong transient increases of GH and cortisol.

Our study may provide an initial indication that ghrelin can exert antidepressant effects in patients with major depression. Ghrelin strongly affected sleep and secretion of GH and cortisol in a partly different way as previously reported in healthy subjects.

The DIAMOND (Depression Improvement Across Minnesota--Offering a New Direction) project is a clinical intervention that was developed and implemented by the Institute for Clinical Systems Improvement (ICSI) in Minnesota beginning in 2008. The ambitious goals of the project were to implement an evidence based model of depression into a variety of settings while changing the reimbursement system for these clinics in order to sustain this model over time. Two years later, the model is in 80 different primary care clinics and data is reported to the state.

A review of the major outcomes from this translation of evidence into practice. Preliminary research on critical factors leading to best outcomes will be offered.

Patients with a diagnosis of Major Depression or Dysthymia and a PHQ-9 score of 10 or greater are eligible for this model of care. Outcome measures include remission rates at six and twelve months. Process measures include the use of the primary tool (PHQ-9), the percentage of eligible patients activated into care management, and drop out or opt out rates. Site visits to all clinics were carried out after implementation by ICSI with preliminary results on best practices.

Results are comparable to those found in randomized controlled trials. As of March 2010, 6-month response averaged 36% (range 8–60%) and 6-month remission averaged 27% (range 7–51%). All intent to treat.

The DIAMOND model was successfully disseminated into diverse settings with excellent results. Factors predicting best clinic outcomes will be reviewed.