Tvangshjemler kan føre til mer tvang

Source at https://www.dagensmedisin.no/tvangshjemler-kan-fore-til-mer-tvang/538388.En praksis med bruk av tepper, bandasjer, borrelåsstropper eller lignende for å sikre pasienter som motsetter seg under transport, kan være svært inngripende – og gir grunn til bekymring

Health professionals' experience of treatment of patients whose community treatment order was revoked under new capacity-based mental health legislation in Norway: qualitative study

Background Norway introduced capacity-based legislation in mental healthcare on 1 September 2017 with the aim of increasing patient autonomy and legal protection and reducing the use of coercion. The new legislation was expected to be particularly important for patients under community treatment orders (CTOs). Aims To explore health professionals’ experiences of how capacity-based legislation affects healthcare services for patients whose compulsory treatment order was revoked as a result of being assessed as having capacity to consent. Method Nine health professionals responsible for treatment and care of patients whose CTO was revoked owing to the new legislation were interviewed in depth from September 2019 to March 2020. We used a hermeneutic approach to the interviews and analysis of the transcripts. Results The participants found that capacity-based legislation raised their awareness of their responsibility for patient autonomy and involvement in treatment and care. They also felt a need for more frequent assessments of patients’ condition and capacity to consent and more flexibility between levels of care. Conclusions The study shows that health professionals found that capacity-based legislation raised their awareness of their responsibility for patient autonomy and involvement in treatment and care. They sought closer dialogue with patients, providing information and advice, and more frequently assessing patients’ condition to adjust treatment and care to enable them to retain their capacity to consent. This could be challenging and required competence, continuity and close collaboration between personnel in different healthcare services at primary and specialist level

Døgnvariasjoner for innleggelser ved akuttpsykiatriske enheter

Akuttpsykiatriske enheter gir øyeblikkelig hjelp til pasienter med særlig vanskelige og kompliserte tilstander med behov utover det som kan ivaretas i kommunehelsetjenesten eller ved distriktspsykiatriske senter (DPS). Flere studier har de siste årene sett på antallet innleggelser og hyppigheten av tvangsbruk i akuttpsykiatriske enheter i Norge (Bjerke et al., 2019; Tøgersen et al., 2015; Wynn, 2018). Bjerke, Gjelstad og Ruud viser at antallet tvangsinnleggelser holdt seg stabilt i perioden 2010 til 2017 (Bjerke et al., 2019). Videre er det funnet at den gjennomsnittlige liggetiden i psykisk helsevern er redusert med 30 % i perioden fra 2009 til 2018 (Statistisk sentralbyrå, 2019). Noen studier har også sett på tidspunkt for innleggelser i akuttpsykiatrien, det vil si når på døgnet pasienter blir lagt inn. Dette har imidlertid ikke blitt undersøkt de siste 10 årene og etter at samhandlingsreformen trådte i kraft (St.meld. nr. 47, 2008). Innleggelser ved akuttpsykiatriske enheter viser noe ulike mønstre. En norsk multisenterstudie fra 2006 der 19 akuttpsykiatriske enheter deltok, viste at gjennomsnittlig 48 % av innleggelsene i akuttpsykiatrien fant sted på dagtid, mens 42 % på kveldstid og 10 % på natt (Gråwe, Hatling & Ruud, 2006). En annen norsk studie fant at 24 % av pasientene ble innlagt mellom klokken (kl.) 16:00 og 22:00, mens 19 % ble lagt inn mellom kl. 22:00 og kl. 08:00, og øvrige innleggelser fant sted på dagtid (Deraas et al., 2006). Videre viste en undersøkelse av 1323 psykiatriske akuttinnleggelser på Lovisenberg Sykehus at 52 % av innleggelsene fant sted på dagtid, altså mellom klokken 08:00 og 16:00 (Berg, 2007). Det ble funnet at 39 % ble innlagt mellom klokken 16:00 og 01:00 og 9 % i tidsrommet 01:00–08:00. Forskjellene mellom tidspunktene var imidlertid ikke signifikante. Hensikten med den nåværende studien er å undersøke hvordan innleggelser i akuttpsykiatriske enheter fordeler seg over døgnet. Vi forventet å finne at flertallet av innleggelsene skjedde på dagtid

Genome-wide interaction study of a proxy for stress-sensitivity and its prediction of major depressive disorder

Individual response to stress is correlated with neuroticism and is an important predictor of both neuroticism and the onset of major depressive disorder (MDD). Identification of the genetics underpinning individual differences in response to negative events (stress-sensitivity) may improve our understanding of the molecular pathways involved, and its association with stress-related illnesses. We sought to generate a proxy for stress-sensitivity through modelling the interaction between SNP allele and MDD status on neuroticism score in order to identify genetic variants that contribute to the higher neuroticism seen in individuals with a lifetime diagnosis of depression compared to unaffected individuals. Meta-analysis of genome-wide interaction studies (GWIS) in UK Biobank (N = 23,092) and Generation Scotland: Scottish Family Health Study (N = 7,155) identified no genome-wide significance SNP interactions. However, gene-based tests identified a genome-wide significant gene, ZNF366, a negative regulator of glucocorticoid receptor function implicated in alcohol dependence (p = 1.48x10-7; Bonferroni-corrected significance threshold p < 2.79x10-6). Using summary statistics from the stress-sensitivity term of the GWIS, SNP heritability for stress-sensitivity was estimated at 5.0%. In models fitting polygenic risk scores of both MDD and neuroticism derived from independent GWAS, we show that polygenic risk scores derived from the UK Biobank stress-sensitivity GWIS significantly improved the prediction of MDD in Generation Scotland. This study may improve interpretation of larger genome-wide association studies of MDD and other stress-related illnesses, and the understanding of the etiological mechanisms underpinning stress-sensitivity

Hair Cortisol in Twins : Heritability and Genetic Overlap with Psychological Variables and Stress-System Genes

A. Palotie on työryhmän jäsen.Hair cortisol concentration (HCC) is a promising measure of long-term hypothalamus-pituitary-adrenal (HPA) axis activity. Previous research has suggested an association between HCC and psychological variables, and initial studies of inter-individual variance in HCC have implicated genetic factors. However, whether HCC and psychological variables share genetic risk factors remains unclear. The aims of the present twin study were to: (i) assess the heritability of HCC; (ii) estimate the phenotypic and genetic correlation between HPA axis activity and the psychological variables perceived stress, depressive symptoms, and neuroticism; using formal genetic twin models and molecular genetic methods, i.e. polygenic risk scores (PRS). HCC was measured in 671 adolescents and young adults. These included 115 monozygotic and 183 dizygotic twin-pairs. For 432 subjects PRS scores for plasma cortisol, major depression, and neuroticism were calculated using data from large genome wide association studies. The twin model revealed a heritability for HCC of 72%. No significant phenotypic or genetic correlation was found between HCC and the three psychological variables of interest. PRS did not explain variance in HCC. The present data suggest that HCC is highly heritable. However, the data do not support a strong biological link between HCC and any of the investigated psychological variables.Peer reviewe

Identification of common genetic risk variants for autism spectrum disorder

Autism spectrum disorder (ASD) is a highly heritable and heterogeneous group of neurodevelopmental phenotypes diagnosed in more than 1% of children. Common genetic variants contribute substantially to ASD susceptibility, but to date no individual variants have been robustly associated with ASD. With a marked sample-size increase from a unique Danish population resource, we report a genome-wide association meta-analysis of 18,381 individuals with ASD and 27,969 controls that identified five genome-wide-significant loci. Leveraging GWAS results from three phenotypes with significantly overlapping genetic architectures (schizophrenia, major depression, and educational attainment), we identified seven additional loci shared with other traits at equally strict significance levels. Dissecting the polygenic architecture, we found both quantitative and qualitative polygenic heterogeneity across ASD subtypes. These results highlight biological insights, particularly relating to neuronal function and corticogenesis, and establish that GWAS performed at scale will be much more productive in the near term in ASD

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

Classical Human Leukocyte Antigen Alleles and C4 Haplotypes Are Not Significantly Associated With Depression

Background The prevalence of depression is higher in individuals with autoimmune diseases, but the mechanisms underlying the observed comorbidities are unknown. Shared genetic etiology is a plausible explanation for the overlap, and in this study we tested whether genetic variation in the major histocompatibility complex (MHC), which is associated with risk for autoimmune diseases, is also associated with risk for depression. Methods We fine-mapped the classical MHC (chr6: 29.6–33.1 Mb), imputing 216 human leukocyte antigen (HLA) alleles and 4 complement component 4 (C4) haplotypes in studies from the Psychiatric Genomics Consortium Major Depressive Disorder Working Group and the UK Biobank. The total sample size was 45,149 depression cases and 86,698 controls. We tested for association between depression status and imputed MHC variants, applying both a region-wide significance threshold (3.9 × 10−6) and a candidate threshold (1.6 × 10−4). Results No HLA alleles or C4 haplotypes were associated with depression at the region-wide threshold. HLA-B*08:01 was associated with modest protection for depression at the candidate threshold for testing in HLA genes in the meta-analysis (odds ratio = 0.98, 95 confidence interval = 0.97–0.99). Conclusions We found no evidence that an increased risk for depression was conferred by HLA alleles, which play a major role in the genetic susceptibility to autoimmune diseases, or C4 haplotypes, which are strongly associated with schizophrenia. These results suggest that any HLA or C4 variants associated with depression either are rare or have very modest effect sizes

Evidence for Increased Genetic Risk Load for Major Depression in Patients Assigned to Electroconvulsive Therapy

Electroconvulsive therapy (ECT) is the treatment of choice for severe and treatment-resistant depression; disorder severity and unfavorable treatment outcomes are shown to be influenced by an increased genetic burden for major depression (MD). Here, we tested whether ECT assignment and response/nonresponse are associated with an increased genetic burden for major depression (MD) using polygenic risk score (PRS), which summarize the contribution of diseaserelated common risk variants. Fifty-one psychiatric inpatients suffering from a major depressive episode underwent ECT. MD-PRS were calculated for these inpatients and a separate population-based sample (n = 3,547 healthy; n = 426 self-reported depression) based on summary statistics from the Psychiatric Genomics Consortium MDD-working group (Cases: n = 59,851; Controls: n = 113,154). MD-PRS explained a significant proportion of disease status between ECT patients and healthy controls (p = .022, R2 = 1.173%); patients showed higher MD-PRS. MD-PRS in population-based depression self-reporters were intermediate between ECT patients and controls (n.s.). Significant associations between MD-PRS and ECT response (50% reduction in Hamilton depression rating scale scores) were not observed. Our findings indicate that ECT cohorts show an increased genetic burden for MD and are consistent with the hypothesis that treatment-resistant MD patients represent a subgroup with an increased genetic risk for MD. Larger samples are needed to better substantiate these findings

A phenome-wide association and Mendelian Randomisation study of polygenic risk for depression in UK Biobank.

Depression is a leading cause of worldwide disability but there remains considerable uncertainty regarding its neural and behavioural associations. Here, using non-overlapping Psychiatric Genomics Consortium (PGC) datasets as a reference, we estimate polygenic risk scores for depression (depression-PRS) in a discovery (N = 10,674) and replication (N = 11,214) imaging sample from UK Biobank. We report 77 traits that are significantly associated with depression-PRS, in both discovery and replication analyses. Mendelian Randomisation analysis supports a potential causal effect of liability to depression on brain white matter microstructure (β: 0.125 to 0.868, pFDR < 0.043). Several behavioural traits are also associated with depression-PRS (β: 0.014 to 0.180, pFDR: 0.049 to 1.28 × 10-14) and we find a significant and positive interaction between depression-PRS and adverse environmental exposures on mental health outcomes. This study reveals replicable associations between depression-PRS and white matter microstructure. Our results indicate that white matter microstructure differences may be a causal consequence of liability to depression