Physical frailty and depressive symptoms are reciprocally related in community-based studies, but its prognostic impact on depressive disorder remains unknown.

A cohort of 378 older persons (≥ 60 years) suffering from a depressive disorder (DSM-IV criteria) was reassessed at two-year follow-up. Depressive symptom severity was assessed every six months with the Inventory of Depressive Symptomatology, including a mood, motivational, and somatic subscale. Frailty was assessed according to the physical frailty phenotype at the baseline examination.

For each additional frailty component, the odds of non-remission was 1.24 [95% CI = 1.01–1.52] (P = 040). Linear mixed models showed that only improvement of the motivational (P < 001) subscale and the somatic subscale (P = 003) of the IDS over time were dependent on the frailty severity.

Physical frailty negatively impacts the course of late-life depression. Since only improvement of mood symptoms was independent of frailty severity, one may hypothesize that frailty and residual depression are easily mixed-up in psychiatric treatment.

To determine the prevalence of metabolic syndrome (MS) in outpatients treated with antipsychotics included in a primary-health-care database.

A cross-sectional study was carried out assessing an administrative outpatients claim-database from 5 primary-health-centers. Subjects on antipsychotics for more than 3 months were included. The control group was formed by the outpatients included in the database without exposition to any antipsychotic drugs. MS was defined according to the modified NCEP-ATP III criteria, and required confirmation of at least 3 of the 5 following components: body mass index >28.8 kg/m2, triglycerides >150 mg/ml, HDL-cholesterol <40 mg/ml (men)/<50 mg/ml (women), blood pressure >130/85 mmHg, and fasting serum glucose >110 mg/dl.

We identified 742 patients [51.5% women, aged 55.1 (20.7) years] treated with first- or second-generation antipsychotics during 27.6 (20.3) months. Controls were 85.286 outpatients [50.5% women, aged 45.5 (17.7) years]. MS prevalence was significantly higher in subjects on antipsychotics: 27.0% (95% CI, 23.8–30.1%) vs. 14.4% (14.1–14.6%); age- and sex-adjusted OR = 1.38 (1.16–1.65, P < 0.001). All MS components, except high blood pressure, were significantly more prevalent in the antipsychotic group, particularly body mass index >28.8 kg/m2: 33.0% (29.6–36.4%) vs. 17.8% (17.6–18.1%), adjusted OR = 1.63 (1.39–1.92, P < 0.001), and low HDL-cholesterol levels: 48.4% (44.8–52.0%) vs. 29.3% (29.0–29.6%); adjusted OR = 1.65 (1.42–1.93, P < 0.001). Compared with the reference population, subjects with schizophrenia or bipolar disorder (BD), but not dementia, showed a higher prevalence of MS.

Compared with the general outpatient population, the prevalence of MS was significantly higher in patients with schizophrenia or BD treated with antipsychotics.

An association between inflammation and behavioral domains of mental disorders is of growing interest. Recent studies reported an association between aggression and inflammation. In this study, we investigated the association between aggressive behavior and inflammatory markers in schizophrenia inpatients.

Adult schizophrenia inpatients without affective symptoms (n = 213) were retrospectively identified and categorized according to their C-reactive protein measurement at admission as either elevated (CRP > 1 mg/dL; n = 57) or normal (CRP < 1 mg/dL; n = 156). The following indicators of aggression were compared: PANSS excitement component (PANSS-EC), restraints and suicidal behavior during hospitalization. Univariate comparisons between elevated and normal CRP levels were performed and multivariate analysis was conducted to control for relevant covariates.

CRP levels significantly correlated with other laboratory markers indicating increased inflammation including leukocyte count and neutrophil to lymphocyte ratio (r = 0.387, P < 0.0001 and r = 0.356, P < 0.0001) respectively. Inpatients with elevated C-reactive protein displayed increased aggressive behavior compared to patients with normal CRP levels (<1 mg/dL). This was manifested by higher rates of restraint during hospitalization (χ2 = 5.22, P = 0.031) and increased PANSS-EC score (U = 5410.5, P = 0.012). Elevated CRP levels were not associated with suicidal behavior. Multivariate analysis revealed that higher PANSS-EC score was associated with elevated CRP after controlling for the covariates age, sex, BMI and smoking.

This study identified a potential biological correlate (inflammation) of a specific behavioral endophenotype (aggression) in schizophrenia inpatients.

This study investigated differences in cognitive performance between middle-aged adults with and without a lifetime history of mood disorder features, adjusting for a range of potential confounders.

Cross-sectional analysis of baseline data from the UK Biobank cohort. Adults aged 40–69 (n = 143,828) were assessed using measures of reasoning, reaction time and memory. Self-reported data on lifetime features of major depression and bipolar disorder were used to construct groups for comparison against controls. Regression models examined the association between mood disorder classification and cognitive performance, adjusting for sociodemographic, lifestyle and clinical confounders.

Inverse associations between lifetime history of bipolar or severe recurrent depression features and cognitive performance were attenuated or reversed after adjusting for confounders, including psychotropic medication use and current depressive symptoms. Participants with a lifetime history of single episode or moderate recurrent depression features outperformed controls to a small (but statistically significant) degree, independent of adjustment for confounders. There was a significant interaction between use of psychotropic medication and lifetime mood disorder features, with reduced cognitive performance observed in participants taking psychotropic medication.

In this general population sample of adults in middle age, lifetime features of recurrent depression or bipolar disorder were only associated with cognitive impairment within unadjusted analyses. These findings underscore the importance of adjusting for potential confounders when investigating mood disorder-related cognitive function.

Cognitive disturbances are widely pronounced in schizophrenia and schizophrenia spectrum disorders. Whilst cognitive deficits are well established in the prodromal phase and are known to deteriorate at the onset of schizophrenia, there is a certain discrepancy of findings regarding the cognitive alterations over the course of the illness.

We bring together the results of the longitudinal studies identified through PubMed which have covered more than 3 years follow-up and to reflect on the potential factors, such as sample characteristics and stage of the illness which may contribute to the various trajectories of cognitive changes.

A summary of recent findings comprising the changes of the cognitive functioning in schizophrenia patients along the longitudinal course of the illness is provided. The potential approaches for addressing cognition in the course of schizophrenia are discussed.

Given the existing controversies on the course of cognitive changes in schizophrenia, differentiated approaches specifically focusing on the peculiarities of the clinical features and changes in specific cognitive domains could shed light on the trajectories of cognitive deficits in schizophrenia and spectrum disorders.

The aim of this study was to assess the prevalence and factors influencing depression in PD patients in a cross-sectional outpatient clinic - based Polish patients sample.

One hundred consecutive PD patients were included in this study; 35 of them fulfilled DSM-IV criteria for Major Depression and its severity was assessed with Montgomery–Asberg Depression Rating Scale (MADRS). A structured interview and a neurological examination, including Hoehn and Yahr scale (H–Y), Schwab–England disability scale, II, III, IV parts of Unified Parkinson's Disease Rating Scale (UPDRS), and Mini-Mental State Examination (MMSE) were performed. The parameters obtained were analysed between the depressed and non-depressed PD patients.

The prevalence of depression in PD in Polish population was established at the level of 35%. PD patients with depression scored significantly higher in all UPDRS scales (except for the subscale of clinical fluctuation) and in H–Y scale. PD with depression was also associated with longer PD duration, higher doses of L-dopa equivalents, patients' age, general impairment of daily living in Schwab and England disability scale, lower MMSE and higher clinical fluctuations. However, those six differences were insignificant.

Depression prevalence rate among PD patients in Polish population is slightly lower than in most of other published studies. This may result from strict selection criteria, use of specific outcome measures and restricted criteria for depression that were applied.

Depression is an important risk factor for suicide. However, other dimensions may contribute to the suicidal risk and to the transition from ideas to acts. We aimed to test the relative involvement of hopelessness, temperament, childhood trauma, and aggression in suicide risk in a large sample of patients with mood disorders.

We assessed 306 patients with major depressive and bipolar disorders for clinical characteristics including hopelessness, temperament, childhood trauma, and aggression. We tested their associations with suicidal ideation and acts using standard univariate/bivariate methods, followed by multivariate logistic regression models.

In multivariate analyses, the loss of expectations subscore of the hopelessness scale was associated with lifetime suicidal ideation but not suicide attempt. Childhood emotional abuse, severity of current depression, and female gender were associated with lifetime suicide attempts, whereas hyperthymic temperament was protective. Only hyperthymic temperament differentiated patients with a history of suicidal ideas vs. those with a history of suicide attempt.

Findings support the association of hopelessness with suicidal ideation and point to considering in suicidal acts not only depression, but also childhood emotional abuse, hyperthymic temperament, and gender.

The present study identified the neural mechanism of risky decision-making in Internet gaming disorder (IGD) under a probability discounting task.

Independent component analysis was used on the functional magnetic resonance imaging data from 19 IGD subjects (22.2 ± 3.08 years) and 21 healthy controls (HC, 22.8 ± 3.5 years).

For the behavioral results, IGD subjects prefer the risky to the fixed options and showed shorter reaction time compared to HC. For the imaging results, the IGD subjects showed higher task-related activity in default mode network (DMN) and less engagement in the executive control network (ECN) than HC when making the risky decisions. Also, we found the activities of DMN correlate negatively with the reaction time and the ECN correlate positively with the probability discounting rates.

The results suggest that people with IGD show altered modulation in DMN and deficit in executive control function, which might be the reason for why the IGD subjects continue to play online games despite the potential negative consequences.

To review the diagnostic validity and utility of mixed depression, i.e. co-occurrence of depression and manic/hypomanic symptoms.

PubMed search of all English-language papers published between January 1966 and December 2006 using and cross-listing key words: bipolar disorder, mixed states, criteria, utility, validation, gender, temperament, depression-mixed states, mixed depression, depressive mixed state/s, dysphoric hypomania, mixed hypomania, mixed/dysphoric mania, agitated depression, anxiety disorders, neuroimaging, pathophysiology, and genetics. A manual review of paper reference lists was also conducted.

By classic diagnostic validators, the diagnostic validity of categorically-defined mixed depression (i.e. at least 2–3 manic/hypomanic symptoms) is mainly supported by family history (the current strongest diagnostic validator). Its diagnostic utility is supported by treatment response (negative effects of antidepressants). A dimensionally-defined mixed depression is instead supported by a non-bi-modal distribution of its intradepression manic/hypomanic symptoms.

Categorically-defined mixed depression may have some diagnostic validity (family history is the current strongest validator). Its diagnostic utility seems supported by treatment response.