Atypical antipsychotics (AAPs) are known to increase the risk of metabolic syndrome (MetS), a predictor for cardiovascular disease and diabetes. This risk differs according to the AAPs.

The objective of this analysis was to examine the incidence of MetS in schizophrenia patients treated with asenapine or olanzapine.

The aim was to estimate the incidence of MetS among schizophrenia patients (DSM-IV criteria) after 52 weeks of exposure to asenapine or olanzapine.

Pooled data from patients completing 52-week extension of randomized trials (041512, 041513, 25544 and A7501014) were included. Patients were treated with asenapine or olanzapine.

The National Cholesterol Education Program, Adult Treatment Panel III (NCEP ATP III) definition of MetS was used, defined as 3 or more of the 5 following risk determinants: waist circumference > 102 cm for male and > 88 cm for female, triglycerides = 150 mg/dL, HDL cholesterol < 40 mg/dL for male and < 50 mg/dL for female, sitting blood pressure ≥ 130/85 mm Hg, or fasting glucose ≥ 110 mg/dL.

Incidence (i.e. new metabolic cases in patients without MetS at baseline) was calculated at week 52.

741 patients were included in this analysis of 52-week studies (asenapine 397, olanzapine 344). After 52 weeks of treatment exposure, the incidence of MetS was significantly higher in olanzapine-treated patients than in asenapine-treated patients (19.44% versus 11.46%, p = 0.01).

These post-hoc analyses confirmed a higher risk of developing a MetS with olanzapine. The incidence of MetS after 52 weeks of treatment with asenapine was found to be significantly lower.

To evaluate the efficacy, safety, and tolerability of fixed-dose agomelatine 25 and 50 mg/d in the treatment of outpatients with obsesive-compulsive disorder (OCD) compared to placebo.

In this 8-week, multicenter, double-blind, parallel-group trial, patients with DSM-IV-defined OCD were randomly assigned (1:1:1) to receive a once-daily dose of agomelatine 25 mg, agomelatine 50 mg, or placebo. The primary efficacy measure was the change from baseline to week 8 in the clinician-rated 17-item Hamilton Depression Rating Scale (HDRS(17)); other efficacy measures were The Yale-Brown Obsessive Compulsive Scale (Y-BOCS) and the Clinical Global Impression scale. The study was conducted between December 2009 and January 2010.

Agomelatine 25 mg/d was more efficacious based on the HDRS(17) total score (P = .01) compared to placebo throughout the treatment period, whereas for agomelatine 50 mg/d, statistically significant reduction in HDRS(17) total score could be observed from weeks 2 to 6 but not at week 8 (P = .144). A higher proportion of patients receiving agomelatine 25 mg/d showed clinical response (P = .013), clinical remission (P = .07), and improvement according to the Clinical Global Impressions-Improvement scale (P = .065) compared to those receiving placebo. No statistically significant difference between patients receiving agomelatine 50 mg/d compared to placebo on clinical response. Both agomelatine doses were safe and well tolerated, although clinically notable aminotransferase elevations were observed transiently in the agomelatine 50 mg/d group.

Agomelatine 50 mg/d provided evidence for its antidepressant efficacy until week 6 and was also safe and well tolerated.

Dyfunctions of prefrontal neuronal circuits contribute to the pathophysiology of depression. Previous studies showed increased functional MRI and EEG connectivity in patients with depression. In this study we investigated a large sample of patients with major depression (n=228) and healthy subjects (n=215).

Spectrotemporal dynamics during resting state with closed eyes were analyzed in sensor and source space to examine functional EEG connectivity (fcEEG) alterations between groups. Quantitative measures of delta, theta, alpha, beta and gamma power, hemispheric asymmetry, coherence, phase and current source density (CSD, eLORETA) analyses were calculated from artifact-free EEG recordings.

EEG theta power was increased in all brain regions in the group of patients with a focus in frontal regions and increased frontal theta and alpha power. Excessive coherence differences were detected in the delta, theta and alpha-bands in frontal, frontal-temporal and frontal-parietal regions. There were changes in phase differences in the delta, theta, alpha-bands between patients and healthy subjects. Differences in CSD were found for the delta, theta, alpha-band in the (rostral and subgenual) anterior cingulate cortex (ACC) with increased CSD in the patients.

The main finding of the present study was an increase in cortical slow-wave activity in sensor and source space in patients with depression revealing marked differences in prefrontal cortical networks. Functional delta, theta and alpha connectivity (coherence and phase) were altered with a predominance in the left hemisphere. Dysfunctions of the ACC, together with alterations in fcEEG may contribute to the pathophysiology of major depression.

Cortisol exerts effects on the brain via two different receptors, producing complex and sometimes opposite effects on the brain structures involved with the different cognitive functions.

To scrutinize the interrelationships between cortisol, cognition and dementia.

Review of the literature and new own findings.

Animal and clinical studies showed an association between increased cortisol and poorer overall cognitive performance, declarative memory, language, processing speed, executive functioning, spatial memory, as well as social memory. High cortisol may exhibit neurotoxic effects on the hippocampus, and exacerbate oxidative injury and amyloid β peptide toxicity. Increased CSF cortisol levels have been found in subjects with dementia and Mild Cognitive Impairment (MCI) due to Alzheimer's disease (AD) compared to control subjects with normal cognition. In MCI due to AD, high CSF cortisol may also predict a more rapid cognitive decline. Higher cortisol levels have been also observed in delirium. Increased cortisol levels interact with inflammatory mediators, neurotransmitters, and growth factors, and may mediate the effects of depression, stressful life events, and personality traits, sleep disturbances, and cardiovascular risk factor on cognitive performance and cognitive decline.

High cortisol levels may exert deleterious effects on cognition and exacerbate AD pathology. Further studies are needed to explore glucocorticoid-based interventions in the management of cognitive disorders.

The authors have not supplied their declaration of competing interest.

Self-Concealment Scale (SCS) is composed of ten items to measure self-concealment, defined as a tendency to conceal from others personal information that one perceives as distressing or negative (Larson and Chastain, 1990).

To investigate the psychometric properties of the SCS-10 Portuguese version and of an adapted version containing two additional items specifically focused on self-concealment related do health problems (physical and psychological)–SCS-12.

The Portuguese version of the SCS-12 and other validated questionnaires designed to evaluate self-reported health, perfectionism and optimism-pessimism were administered to a convenience sample of 555 adults from the community (60.5% females; mean age = 43.49 ± 10.565).

The SCS-10 and SCS-12 Cronbach's alphas were α < 0.80. In both versions, all the items contribute to the internal consistency. The factor analysis, following the Kaiser and the Cattel's Scree Plot criteria, revealed that SCS-10 is unidimensional and that SCS-12 reliably and validly evaluates two dimensions: F1 Keeping secrets (Explained variance = 48.60%; α = 0.816), F2 Personal concealment including health problems (9.65%; α = 0.797). The pattern of correlations of the SCS dimensional and total scores was as follow: negative low correlations with physical health (@−0.20), negative moderate correlations with psychological health (@–.30), moderate correlations with self-oriented perfectionism, social-prescribed perfectionism, pessimism (@0.25) and optimism (@−0.20).

The Portuguese versions of SCS have good reliability and validity (construct and convergent-divergent). The factorial structure partially overlaps with the original. SCS could be useful for research proposes, namely in an ongoing project on the role of the mentioned personality traits on illness and health behavior.

The authors have not supplied their declaration of competing interest.

No significant relationships.

Recognition of cognitive deficits in old-age depression is especially important since they contribute to poor function outcome, have strong implications for coping abilities and treatment compliance. However, substantial variability in cognitive deficits among older depressed persons has been reported. Clinical and demographic characteristics are likely to have contributed to inconsistencies in previous findings.

To assess effects of unipolar depression on cognitive performance in a population-based sample of elderly persons (60+ years).

An extensive cognitive test battery was administered. Eighty-nine persons fulfilled ICD-10 criteria for unipolar depression (mild, n=48; moderate; n=38, severe; n=3) after thorough screening for dementia (DSM-IV criteria), psychiatric comorbidities, antidepressant pharmacotherapy, and lastly preclinical dementia.

Unipolar old-age depression was associated with deficits in processing speed, attention, executive function, verbal fluency, and episodic free recall. No depression-related deficits were observed in short-term memory, semantic memory, or spatial ability. Increasing age did not exacerbate the cognitive deficits in old-age depression. The cognitive deficits remained significant after exclusion of persons with preclinical dementia, except free recall, where performance differences were at trend level.

Cognitive deficits in unipolar old-age depression involve a number of cognitive domains, and are also present among persons with mild depression. Importantly, no statistically significant performance differences between mild and moderate/severe depression were observed. Given the prevalence of depression in older populations, the impact of this disorder on cognitive functioning may be relatively large at the population level.

Brain-derived neurotrophic factor (BDNF) plays an important role in depression and sleep disorders. It influences the inflammatory process and may affect the interactions between psychological state and gastrointestinal symptoms.

The study aimed to compare BDNF concentrations in the group of Crohn’s disease (CD), ulcerative colitis (UC) patients, and healthy control (HC), as well as to correlate it with the severity of depression and insomnia.

The study included 94 inflammatory bowel disease patients (IBD, 57 CD, and 37 UC) and 26 HC. Each participant completed the following questionnaires: Pittsburgh Sleep Quality Index (PSQI), Athens insomnia scale (AIS), and Beck Depression Inventory (BDI). BDNF protein concertation measurements were performed using ELISA. Funding: National Science Centre, Poland-2018/31/N/NZ5/03715.

CD patients had a higher serum level of BDNF (22.5 ng/mL, IQR:17.5-28.5) than UC patients (19.1 ng/mL, IQR:12.3-24.6; p=0.045). CD group had higher BDNF concentrations than HC (17.5 ng/mL, IQR:13.2-23.8; p=0.010), but no such differences were found between UC and HC groups (p=0.544). A positive correlation was found between AIS and BDNF among IBD (r=0.22, p=0.035). Additionally, patients, who obtained high BDI scores (>7 points) had lower BDNF concentrations than others (p=0.004). The patients with long sleep latency (>10 min) achieved a higher BDNF level than others (p=0.038). However. BDNF level did not correlate with PSQI results.

BDNF serum level is increased in CD, but not in UC patients. Overall, the severity of insomnia symptoms correlates positively with BDNF levels. Future research should focus on the further explanation of those observations.

In Correctional Institutions of Kosovo (CIK), the rate of suicide and attempted suicide is low (in the last six years have been six suicide).

Disturbing is the fact that during the period October 2007 to January 2009 at the Lipjan Detention Center (LDC) have been nine suicide and three attempted suicide, while in all other correctional institutions has not happened any suicide and only one attempted suicide. This level is to high when we consider the fact that the capacity of LDC is approximately 200 prisoners, while in all other correctional institutions have about 1500 prisoners.

The objective is to find reasons for such a high level of suicide and attempted suicide in LDC.

The aim is to return the low level of suicidal behavior in LDC.

Mapping:

1. 1. Survey documentation

2. 2. Interviews

3. 3. Focus groups

1. 1. Lack of detection of cases at risk for suicide during admission.

2. 2. Inadequate administrative and health management.

3. 3. Insufficient communication between staff and prisoners

Better management in early detection of cases Creation of a multidisciplinary team for management of cases referred as risky for suicide