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The Health of the nation outcome scales (HoNOS)  were designed to measure the health and social functioning of adults with severe mental health problems. They form part of the English mental health minimum data set and are recommended by the department of health and are part of the attempt to develop “payment by results” (PbR) for mental health . They are also widely used in Australia, New Zealand and Canada [3, 4], and have also been used in Europe . Although they are widely used there are still questions about their psychometric validity and their ability to predict anything useful.
Previous studies in individual countries have identified inconsistent predictors of length of stay (LoS) in psychiatric inpatient units. This may reflect methodological inconsistencies across studies or true differences of predictors. In this study we assessed predictors of LoS in five European countries and explored whether their effect varies across countries.
Prospective cohort study. All patients admitted over 14 months to 57 psychiatric inpatient units in Belgium, Germany, Italy, Poland and United Kingdom were screened. Putative predictors were collected from medical records and in face-to-face interviews and tested for their association with LoS.
Average LoS varied from 17.9 days in Italy to 55.1 days in Belgium. In the overall sample being homeless, receiving benefits, social isolation, diagnosis of psychosis, greater symptom severity, substance use, history of previous admission and being involuntarily admitted predicted longer LoS. Several predictors showed significant interaction effects with countries in predicting LoS. One variable, homelessness, predicted a different LoS even in opposite directions, whilst for other predictors the direction of the association was the same, but the strength of the association with LoS varied across countries.
The same patient characteristics have a different impact on LoS in different contexts. Thus, although some predictor variables related to clinical severity and social dysfunction appear of generalisable relevance, national studies on LoS are required to understand the complex influence of different patient characteristics on clinical practice in the given contexts.
There is irrefutable evidence that routine physical activity or exercise can offer considerable health benefits to individuals living with various mental disorders. However, it is not clear what effect physical activity has on the symptoms of Tourette syndrome. Despite a paucity of evidence, physical activity or exercise has already been recommended by various health organizations for the management of tics. We provide a systematic review of the effects of physical activity or exercise on tic symptomology in individuals with Tourette syndrome. Major electronic databases were searched for all available publications before August 2017. Keywords and MeSH terms included “physical activity” or “exercise” or “exercise therapy” or “physical exertion” or “sports” and “tics” or “tic disorders” or “Tourette.” Eight studies were included, the majority of which were case reports. Despite a number of methodological limitations of the included studies, the review points to a trend that the effects of acute physical activity are intensity-dependent, where light intensity may alleviate and vigorous intensity may exacerbate tics. Chronic physical activity, however, appears to reduce the severity of tics even at higher intensity. Several physiological mechanisms may explain the differential effects of acute and chronic physical activity in Tourette syndrome. Future randomized controlled studies should better characterize the effects of different intensities and types of physical activity in Tourette syndrome.
The 22q11.2 deletion syndrome (22q11DS) is the most common genetic syndrome associated with schizophrenia. The goal of this study was to evaluate longitudinally the interaction between neurocognitive functioning, the presence of subthreshold psychotic symptoms (SPS) and conversion to psychosis in individuals with 22q11DS. In addition, we attempted to identify the specific neurocognitive domains that predict the longitudinal evolution of positive and negative SPS, as well as the effect of psychiatric medications on 22q11DS psychiatric and cognitive developmental trajectories.
Forty-four participants with 22q11DS, 19 with Williams syndrome (WS) and 30 typically developing (TD) controls, age range 12–35 years, were assessed at two time points (15.2 ± 2.1 months apart). Evaluation included the Structured Interview for Prodromal Symptoms (SIPS), structured psychiatric evaluation and the Penn Computerized Neurocognitive Battery (CNB).
22q11DS individuals with SPS had a yearly conversion rate to psychotic disorders of 8.8%, compared to none in both WS and TD controls. Baseline levels of negative SPS were associated with global neurocognitive performance (GNP), executive function and social cognition deficits, in individuals with 22q11DS, but not in WS. Deficits in GNP predicted negative SPS in 22q11DS and the emergence or persistence of negative SPS. 22q11DS individuals treated with psychiatric medications showed significant improvement in GNP score between baseline and follow-up assessments, an improvement that was not seen in untreated 22q11DS.
Our results highlight the time-dependent interplay among positive and negative SPS symptoms, neurocognition and pharmacotherapy in the prediction of the evolution of psychosis in 22q11DS.
Problem-solving therapy (PST) is one of the best examined types of psychotherapy for adult depression. No recent meta-analysis has examined the effects of PST compared to control groups or to other treatments. We wanted to verify whether PST is effective, whether effects are comparable to those of other treatments, and whether we could identify the possible sources of high heterogeneity that was found in earlier meta-analyses.
We conducted systematic searches in bibliographical databases, including PubMed, PsycInfo, Embase and the Cochrane database of randomized trials.
We included 30 randomized controlled trials on PST (with 3530 patients), in which PST was compared to control conditions, with other therapies, and with pharmacotherapy. We could compare these 30 trials on PST also with 259 trials on other psychotherapies for adult depression. The effect size of PST versus control groups was g = 0.79 (0.57–1.01) with very high heterogeneity (I2 = 84; 95% CI: 77–88). The effect size from the 9 studies with low risk of bias was g = 0.34 (95% CI: 0.22–0.46) with low heterogeneity (I2 = 32; 95% CI: 0–68), which is comparable to the effects of other psychotherapies. PST was a little more effective than other therapies in direct comparisons, but that may be explained by the considerable number of studies with researcher allegiance towards PST. In meta-regression analyses of all controlled studies, no significant difference between PST and other therapies was found.
PST is probably an effective treatment for depression, with effect sizes that are small, but comparable to those found for other psychological treatments of depression.
The dominating hypothesis among numerous hypotheses explaining the pathogenesis of depressive disorders (DD) is the one involving oxidative and nitrosative stress. In this study, we examined the association between single-nucleotide polymorphisms of the genes encoding SOD2 (superoxide dismutase 2), CAT (catalase), GPx4 (glutathione peroxidase 4), NOS1 (nitric oxide synthase 1), NOS2 (nitric oxide synthase 2), and the development of depressive disorders. Our study was carried out on the DNA isolated from peripheral blood collected from 281 depressed patients and 229 controls. Using TaqMan probes, we genotyped the following six polymorphisms: c.47T > C (p.Val16Ala) (rs4880) in SOD2, c.-89A > T (rs7943316) in CAT, c.660T > C (rs713041) in GPx4, c.-420-34221G > A (rs1879417) in NOS1, c.1823C > T (p.Ser608Leu) (rs2297518), and c.-227G > C (rs10459953) in NOS2. We found that the T/T genotype of the c.47T > C polymorphism was linked with an increased risk of depression. Moreover, the T/T genotype and T allele of c.660T > C increased the risk of DD occurrence, while the heterozygote and C allele decreased this risk. On the other hand, we discovered that the A/A genotype of c.-89A > T SNP was associated with a reduced risk of DD, while the A/T genotype increased this risk. We did not find any correlation between the genotypes/alleles of c.-420-34221G > A, c.1823C > T, and c.-227G > C, and the occurrence of DD. In addition, gene-gene and haplotype analyses revealed that combined genotypes and haplotypes were connected with the disease. Moreover, we found that sex influenced the impact of some SNPs on the risk of depression. Concluding, the studied polymorphisms of SOD2, CAT and GPx4 may modulate the risk of depression. These results support the hypothesis that oxidative and nitrosative stresses are involved in the pathogenesis of depressive disorders.
Psychiatric inpatient treatment is increasingly performed in settings with locked doors. However, locked wards have well-known disadvantages and are ethically problematic. In addition, recent data challenges the hypothesis that locked wards provide improved safety over open-door settings regarding suicide, absconding and aggression. Furthermore, there is evidence that the introduction of an open-door policy may lead to short-term reductions in involuntary measures. The aim of this study was to assess if the introduction of an open-door policy is associated with a long-term reduction of the frequency of seclusion and forced medication.
In this 6-year, hospital-wide, longitudinal, observational study, we examined the frequency of seclusion and forced medication in 17,359 inpatient cases admitted to the Department of Adult Psychiatry, Universitäre Psychiatrische Kliniken (UPK) Basel, University of Basel, Switzerland. In an approach to enable a less restrictive policy, six previously closed psychiatric wards were permanently opened beginning from August 2011. During this process, a systematic change towards a more patient-centered and recovery-oriented care was applied. Statistical analysis consisted of generalized estimating equations (GEE) models.
In multivariate analyses controlling for potential confounders, the implementation of an open-door policy was associated with a continuous reduction of seclusion (from 8.2 to 3.5%; ηp2 = 0.82; odds ratio: 0.88) and forced medication (from 2.4 to 1.2%; ηp2 = 0.70; odds ratio: 0.90).
This underlines the potential of the introduction of an open-door policy to attain a long-term reduction in involuntary measures.
Considering that specific genetic profiles, psychopathological conditions and neurobiological systems underlie human behaviours, the phenotypic differentiation of obese patients according to eating behaviours should be investigated. The aim of this study was to classify obese patients according to their eating behaviours and to compare these clusters in regard to psychopathology, personality traits, neurocognitive patterns and genetic profiles.
A total of 201 obese outpatients seeking weight reduction treatment underwent a dietetic visit, psychological and psychiatric assessment and genotyping for SCL6A2 polymorphisms. Eating behaviours were clustered through two-step cluster analysis, and these clusters were subsequently compared.
Two groups emerged: cluster 1 contained patients with predominantly prandial hyperphagia, social eating, an increased frequency of the long allele of the 5-HTTLPR and low scores in all tests; and cluster 2 included patients with more emotionally related eating behaviours (emotional eating, grazing, binge eating, night eating, post-dinner eating, craving for carbohydrates), dysfunctional personality traits, neurocognitive impairment, affective disorders and increased frequencies of the short (S) allele and the S/S genotype.
Aside from binge eating, dysfunctional eating behaviours were useful symptoms to identify two different phenotypes of obese patients from a comprehensive set of parameters (genetic, clinical, personality and neuropsychology) in this sample. Grazing and emotional eating were the most important predictors for classifying obese patients, followed by binge eating. This clustering overcomes the idea that ‘binging’ is the predominant altered eating behaviour, and could help physicians other than psychiatrists to identify whether an obese patient has an eating disorder. Finally, recognising different types of obesity may not only allow a more comprehensive understanding of this illness, but also make it possible to tailor patient-specific treatment pathways.
Weight gain among psychiatric inpatients is a widespread phenomenon. This change in body mass index (BMI) can be caused by several factors. Based on recent research, we assume the following factors are related to weight gain during psychiatric inpatient treatment: psychiatric medication, psychiatric diagnosis, sex, age, weight on admission and geographic region of treatment.
876 of originally recruited 2328 patients met the criteria for our analysis. Patients were recruited and examined in mental health care centres in Nigeria (N=265), Japan (N=145) and Western-Europe (Denmark, Germany and Switzerland; N=466).
There was a significant effect of psychiatric medication, psychiatric diagnoses and geographic region, but not age and sex, on BMI changes. Geographic region had a significant effect on BMI change, with Nigerian patients gaining significantly more weight than Japanese and Western European patients. Moreover, geographic region influenced the type of psychiatric medication prescribed and the psychiatric diagnoses. The diagnoses and psychiatric medication prescribed had a significant effect on BMI change.
In conclusion, we consider weight gain as a multifactorial phenomenon that is influenced by several factors. One can discuss a number of explanations for our findings, such as different clinical practices in the geographical regions (prescribing or admission strategies and access-to-care aspects), as well as socio-economic and cultural differences.
The aim of this observational study was to investigate the relationship between metabolic factors and use of selective serotonin reuptake inhibitors (SSRIs) combined with olanzapine, quetiapine or risperidone.
Data from the Norwegian Thematically Organized Psychosis study, a cross-sectional study on 1301 patients with schizophrenia (n=868) or bipolar disorder (n=433), were analyzed. As exposure variables in the linear regression model were included the dose or serum concentration of SSRIs (n=280) and of olanzapine (n=398), quetiapine (n=234) or risperidone (n=128). The main outcome variables were levels of total cholesterol, low and high density lipoprotein (LDL and HDL) cholesterol, triglycerides and glucose.
One defined daily dose (DDD) per day of an SSRI in addition to olanzapine was associated with an increase in total cholesterol of 0.16 (CI 0.01 to 0.32) mmol/L (P=0.042) and an increase in LDL-cholesterol of 0.17 (CI 0.02 to 0.31) mmol/L (P=0.022). An SSRI serum concentration in the middle of the reference interval in addition to quetiapine was associated with an increase in total cholesterol of 0.39 (CI 0.10 to 0.68) mmol/L (P=0.011) and an increase in LDL-cholesterol of 0.29 (0.02 to 0.56) mmol/L (P=0.037). There were no such effects when combined with risperidone.
The findings indicate only minor deteriorations of metabolic variables associated with treatment with an SSRI in addition to olanzapine and quetiapine, and none when combined with risperidone. These results suggest that SSRIs can be used in combination with antipsychotics, and that the possible increase in cardiovascular risk is negligible.
To provide an overview on the magnitude of the impact of schizophrenia on the healthcare system in Europe and to gain a better understanding on the most important factors influencing the variation of costs.
Studies reporting costs and healthcare utilization among patients with schizophrenia were searched in MEDLINE (via Scopus), EMBASE (via Scopus) and Cochrane Database of Systematic Reviews on 19th January 2017.
Twenty-three studies, from the 1075 references initially identified, were included in this review. The annual cost per patient ranged from €533 in Ukraine to €13,704 in the Netherlands. Notably drug costs contributed to less than 25% of the direct healthcare cost per patient in every country, which might be explained by similar pharmaceutical prices among countries due to the reference pricing system applied in Europe. Inpatient costs were the largest component of health service costs in the majority of the countries. Despite methodological heterogeneity across studies, four major themes could be identified (age, severity of symptoms, continuation of treatment/persistence, hospitalization) that have substantial impact on the costs of schizophrenia.
Schizophrenia represents a substantial cost for the healthcare system in Europe driven by the high cost per patient. Substantial savings could potentially be achieved by increasing investment in the following areas: (1) reducing the number of hospitalizations e.g. by increasing the efficiency of outpatient care; (2) working out interventions targeted at specific symptoms; (3) improving patient persistence and adherence in antipsychotic therapy.