Suicide risk assessment in a large public mental health service: do suicide risk classifications identify those at risk?

INTRODUCTION: Risk assessment tools are routinely used to identify patients at high risk. There is increasing evidence that these tools may not be sufficiently accurate to determine the risk of suicide of people, particularly those being treated in community mental health settings. METHODS: An outcome analysis for case serials of people who died by suicide between January 2014 and December 2016 and had contact with a public mental health service within 31 days prior to their death. RESULTS: Of the 68 people who had contact, 70.5% had a formal risk assessment. Seventy-five per cent were classified as low risk of suicide. None were identified as being at high risk. While individual risk factors were identified, these did not allow to differentiate between patients classified as low or medium. DISCUSSION: Risk categorisation contributes little to patient safety. Given the dynamic nature of suicide risk, a risk assessment should focus on modifiable risk factors and safety planning rather than risk prediction. CONCLUSION: The prediction value of suicide risk assessment tools is limited. The risk classifications of high, medium or low could become the basis of denying necessary treatment to many and delivering unnecessary treatment to some and should not be used for care allocation.

How health care systems let our patients down: a systematic review into suicide deaths.

PURPOSE: To synthesize the literature in relation to findings of system errors through reviews of suicide deaths in the public mental health system. DATA SOURCES: A systematic narrative meta-synthesis using the PRISMA methodology was conducted. STUDY SELECTION: All English language articles published between 2000 and 2017 that reported on system errors identified through reviews of suicide deaths were included. Articles that reported on patient factors, contact with General Practitioners or individual cases were excluded. DATA EXTRACTION: Results were extracted and summarized. An overarching coding framework was developed inductively. This coding framework was reapplied to the full data set. RESULTS OF DATA SYNTHESIS: Fourteen peer reviewed publications were identified. Nine focussed on suicide deaths that occurred in hospital or psychiatric inpatient units. Five studies focussed on suicide deaths while being treated in the community. Vulnerabilities were identified throughout the patient's journey (i.e. point of entry, transitioning between teams, and point of exit with the service) and centred on information gathering (i.e. inadequate and incomplete risk assessments or lack of family involvement) and information flow (i.e. transitions between different teams). Beyond enhancing policy, guidelines, documentation and regular training for frontline staff there were very limited suggestions as to how systems can make it easier for staff to support their patients. CONCLUSIONS: There are currently limited studies that have investigated learnings and recommendations. Identifying critical vulnerabilities in systems and to be proactive about these could be one way to develop a highly reliable mental health care system.

PROMISE. Beyond frontiers.

The concepts underlying the PROMISE initiative are described. This initiative to implement more humane healthcare is now developing from a local initiativein Cambridge to a global movement.

Schizophrenia delays and alters maturation of the brain in adolescence.

Early-onset schizophrenia appears to be clinically more severe than the adult-onset form of the disease. In a previous study, we showed that anatomically related grey and white matter abnormalities found in adolescents patients were larger and more widespread than what had been reported in the literature on adult schizophrenia. Particularly, we found novel structural abnormalities in the primary sensorimotor and premotor systems. Here, we tested alternative hypotheses: either this striking sensorimotor-related pattern is an artefact due to a better sensitivity of the methods, or apparent greater structural abnormalities in the early-onset population are specifically associated with earlier disease onset. Then, if we were to find such characteristic structural pattern, we would test whether these anatomical abnormalities would remain static or, conversely, show dynamic changes in the still developing brain. To address these questions, we combined a cross-sectional study of brain structure for adolescent-onset patients (n = 25) and adult-onset patients (n = 35) and respective matched healthy subjects with a longitudinal study of adolescent-onset patients (n = 12, representative subset of the cross-sectional group) and matched healthy controls for >2 years. Looking at differences between adolescent and adult patients' grey matter volume and white matter microstructure abnormalities, we first confirmed the specificity (especially in motor-related areas) and the greater severity of structural abnormalities in the adolescent patients. Closer examination revealed, however, that such greater anomalies seemed to arise because adolescent patients fail to follow the same developmental time course as the healthy control group. Longitudinal analysis of a representative subset of the adolescent patient and matched healthy populations corroborated the delayed and altered maturation in both grey and white matters. Structural abnormalities specific to adolescent-onset schizophrenia in the sensori-motor cortices and corticospinal tract were less marked or even disappeared within the longitudinal period of observation, grey matter abnormalities in adolescent patients evolving towards the adult-onset pattern as defined by recent meta-analyses of adult schizophrenia. Combining cross-sectional adolescent and adult datasets with longitudinal adolescent dataset allowed us to find a unique, abnormal trajectory of grey matter maturation regardless of the age at onset of symptoms and of disease duration, with a lower and later peak than for healthy subjects. Taken together, these results suggest common aetiological mechanisms for adolescent- and adult-onset schizophrenia with an altered neurodevelopmental time course in the schizophrenic patients that is particularly salient in adolescence.

Bilateral generic working memory circuit requires left-lateralized addition for verbal processing.

According to the Baddeley-Hitch model, phonological and visuospatial representations are separable components of working memory (WM) linked by a central executive. The traditional view that the separation reflects the relative contribution of the 2 hemispheres (verbal WM--left; spatial WM--right) has been challenged by the position that a common bilateral frontoparietal network subserves both domains. Here, we test the hypothesis that there is a generic WM circuit that recruits additional specialized regions for verbal and spatial processing. We designed a functional magnetic resonance imaging paradigm to elicit activation in the WM circuit for verbal and spatial information using identical stimuli and applied this in 33 healthy controls. We detected left-lateralized quantitative differences in the left frontal and temporal lobe for verbal > spatial WM but no areas of activation for spatial > verbal WM. We speculate that spatial WM is analogous to a "generic" bilateral frontoparietal WM circuit we inherited from our great ape ancestors that evolved, by recruitment of additional left-lateralized frontal and temporal regions, to accommodate language.

Confirmation of the genetic association between the U2AF homology motif (UHM) kinase 1 (UHMK1) gene and schizophrenia on chromosome 1q23.3.

UHMK1 has previously been implicated as a susceptibility gene for schizophrenia in the 1q23.3 region by significant evidence of allelic and haplotypic association between schizophrenia and several genetic markers at UHMK1 in a London-based case-control sample. Further fine mapping of the UHMK1 gene locus in the University College London schizophrenia case-control sample was carried out with tagging SNPs. Two additional SNPs were found to be associated with schizophrenia (rs6604863 P = 0.02, rs10753578 P = 0.017). Tests of allelic and haplotypic association were then carried out in a second independent sample from Aberdeen consisting of 858 individuals with schizophrenia and 591 controls. Two of these SNPs also showed association in the Aberdeen sample (rs7513662 P = 0.0087, rs10753578 P = 0.022) and several haplotypes were associated (global permutation P = 0.0004). When the UCL and Aberdeen samples were combined three SNPs (rs7513662 P = 0.0007, rs6427680 P = 0.0252, rs6694863 P = 0.015) and several haplotypes showed association (eg HAP-A, HAP-B, HAP-C permutation P = 0.00005). The finding of allelic association with markers in the UHMK1 gene might help explain why it has not been possible, despite great effort, to satisfactorily confirm previously reported associations between schizophrenia and the genes RGS4 and NOS1AP/CAPON. These genes flank UHMK1 and all three loci are within a 700 kb region showing linkage to schizophrenia. The confirmation of association between UHMK1 and schizophrenia, rather than RGS4 and NOS1AP in the London sample, points to the possibility that previous efforts to accurately fine map a gene in the 1q23.3 region have lacked accuracy or may have suffered from methodological flaws.

5HT(3) antagonism abolishes the emotion potentiated startle effect in humans.

RATIONALE: The serotonergic system has been implicated in emotional processing in animals and humans. Although the contribution of different receptor subtypes has been hypothesised, there have been few direct tests of this in human subjects. OBJECTIVES: The current study aimed to explore the involvement of the serotonin type 3 (5HT3) receptor subtype in a battery of emotional processing tasks previously found to be sensitive to SSRI administration. MATERIALS AND METHODS: Healthy volunteers were randomised to receive the 5HT3 antagonist, ondansetron (12 mg, oral), or placebo in a double blind between groups design. Emotional processing was assessed using three tasks: affective modulation of the startle reflex, emotional categorisation and memory and facial expression recognition. Subjective state ratings, blood pressure and pulse were also collected before and after ondansetron and placebo. RESULTS: Ondansetron was well tolerated and did not affect subjective measures of mood, anxiety or well-being in these healthy volunteers. However, the emotion potentiated effect was abolished in the volunteers receiving ondansetron. Facial expression recognition and emotional memory were not significantly affected. CONCLUSIONS: These results suggest an involvement of 5HT3 receptors in certain aspects of fear processing in humans. These effects are consistent with anxiolytic actions of 5HT3 antagonism in animal models and suggest that the 5HT3 receptor may play a role in the effects of serotonergic manipulations on fear and anxiety.

Long-term hospitalizations for schizophrenia in the Czech Republic 1998-2012.

Deinstitutionalization has not been pursued in the post-communist Europe until recently. The population of psychiatric patients institutionalized in the regional mental hospitals is, however, largely understudied. The aim of this study is to assess discharges of long-term inpatients with schizophrenia from Czech psychiatric hospitals and to analyse re-hospitalizations within this group. The nationwide register of all-cause inpatient hospitalizations was merged with the nationwide register of all-cause deaths on an individual level basis. Descriptive statistics, survival analysis and logistic regression were performed. 3601 patients with schizophrenia previously hospitalized for more than a year were discharged from Czech mental hospitals between 1998 and 2012. This included 260 patients hospitalized for >20years. Nearly one fifth (n=707) of the long-term patients died during the hospitalization; and discharges of 19.36% (n=697) were only administrative in their nature. Out of 2197 truly discharged patients, 14.88% (n=327) were re-hospitalized within 2weeks after the discharge. The highest odds of rehospitalization were associated with being discharged against medical advice (OR 5.27, CI: 3.77-7.35, p<0.001). These data are important for the ongoing mental health care reforms in the Czech Republic and other countries in the Central and Eastern Europe.

Serotonin and dopamine play complementary roles in gambling to recover losses.

Continued gambling to recover losses--'loss chasing'--is a prominent feature of social and pathological gambling. However, little is known about the neuromodulators that influence this behavior. In three separate experiments, we investigated the role of serotonin activity, D(2)/D(3) receptor activity, and beta-adrenoceptor activity on the loss chasing of age and IQ-matched healthy adults randomized to treatment or an appropriate control/placebo. In Experiment 1, participants consumed amino-acid drinks that did or did not contain the serotonin precursor, tryptophan. In Experiment 2, participants received a single 176 µg dose of the D(2)/D(3) receptor agonist, pramipexole, or placebo. In Experiment 3, participants received a single 80 mg dose of the beta-adrenoceptor blocker, propranolol, or placebo. Following treatment, participants completed a computerized loss-chasing game. Mood and heart rate were measured at baseline and following treatment. Tryptophan depletion significantly reduced the number of decisions made to chase losses, and the number of consecutive decisions to chase, in the absence of marked changes in mood. By contrast, pramipexole significantly increased the value of losses chased and diminished the value of losses surrendered. Propranolol markedly reduced heart rate, but produced no significant changes in loss-chasing behavior. Loss chasing can be thought of as an aversively motivated escape behavior controlled, in part, by the marginal value of continued gambling relative to the value of already accumulated losses. Serotonin and dopamine appear to play dissociable roles in the tendency of individuals to gamble to recover, or to seek to 'escape' from, previous losses. Serotonergic activity seems to promote the availability of loss chasing as a behavioral option, whereas D(2)/D(3) receptor activity produces complex changes in the value of losses judged worth chasing. Sympathetic arousal, at least as mediated by beta-adrenoceptors, does not play a major role in laboratory-based loss-chasing choices.