Restraint in mental health care has negative consequences, and guidelines/policies calling for its reduction have emerged internationally. However, there is tension between reducing restraint and maintaining safety. In order to reduce restraint, it is important to gain an understanding of the experience for all involved. The aim of the present study was to improve understanding of the experience of restraint for patients and staff with direct experience and witnesses. Interviews were conducted with 13 patients and 22 staff members from one UK National Health Service trust. The overarching theme, 'is restraint a necessary evil?', contained subthemes fitting into two ideas represented in the quote: 'it never is very nice but…it's a necessary evil'. It 'never is very nice' was demonstrated by the predominantly negative emotional and relational outcomes reported (distress, fear, dehumanizing, negative impact on staff/patient relationships, decreased job satisfaction). However, a common theme from both staff and patients was that, while restraint is 'never very nice', it is a 'necessary evil' when used as a last resort due to safety concerns. Mental health-care providers are under political pressure from national governments to reduce restraint, which is important in terms of reducing its negative outcomes for patients and staff; however, more research is needed into alternatives to restraint, while addressing the safety concerns of all parties. We need to ensure that by reducing or eliminating restraint, mental health wards neither become, nor feel, unsafe to patients or staff.

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.

Continued gambling to recover lossesF'loss chasing'Fis 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 mg 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.

Introduction Physical restraint has negative consequences for all involved, and international calls for its reduction have emerged. Some restraint reduction interventions have been developed, but limited qualitative research explores suggestions on how to reduce physical restraint (and feasibility issues with implementation) from those directly involved. Aims To explore mental health patients' and staff members' suggestions for reducing physical restraint. Methods Interviews were conducted with 13 inpatients and 22 staff members with experience of restraint on adult mental health inpatient wards in one UK National Health Service Trust. Results Findings centred on four overarching themes: improving communication and relationships between staff/patients; making staff-related changes; improving ward environments/spaces; and having more activities. However, concerns were raised around practicalities/feasibility of their implementation. Discussion Continued research is needed into best ways to reduce physical restraint, with an emphasis on feasibility/practicality and how to make time in busy ward environments. Implications for Practice Improving communication and relationships between staff/patients, making staffing-related changes, improving ward environments and providing patient activities are central to restraint reduction in mental healthcare. However, fundamental issues related to understaffing, high staff turnover and lack of time/resources need addressing in order for these suggestions to be successfully implemented.