Aggression on the psychiatric ward: Prevalence and risk factors. A systematic review of the literature.

INTRODUCTION: On psychiatric wards, aggressive behaviour displayed by patients is common and problematic. Understanding factors associated with the development of aggression offers possibilities for prevention and targeted interventions. This review discusses factors that contribute to the development of aggression on psychiatric wards. METHOD: In Pubmed and Embase, a search was performed aimed at: prevalence data, ward characteristics, patient and staff factors that are associated with aggressive behaviour and from this search 146 studies were included. RESULTS: The prevalence of aggressive behaviour on psychiatric wards varied (8-76%). Explanatory factors of aggressive behaviour were subdivided into patient, staff and ward factors. Patient risk factors were diagnosis of psychotic disorder or bipolar disorder, substance abuse, a history of aggression, younger age. Staff risk factors included male gender, unqualified or temporary staff, job strain, dissatisfaction with the job or management, burn-out and quality of the interaction between patients and staff. Staff protective factors were a good functioning team, good leadership and being involved in treatment decisions. Significant ward risk factors were a higher bed occupancy, busy places on the ward, walking rounds, an unsafe environment, a restrictive environment, lack of structure in the day, smoking and lack of privacy. CONCLUSION: Despite a lack of prospective quantitative data, results did show that aggression arises from a combination of patient factors, staff factors and ward factors. Patient factors were studied most often, however, besides treatment, offering the least possibilities in prevention of aggression development. Future studies should focus more on the earlier stages of aggression such as agitation and on factors that are better suited for preventing aggression such as ward and staff factors. Management and clinicians could adapt staffing and ward in line with these results.

Cause-specific mortality among patients with psychosis: disentangling the effects of age and illness duration.

BACKGROUND: There is a large mortality gap between patients with a nonaffective psychotic disorder and those in the general population, is associated with both natural and nonnatural death causes. OBJECTIVE: This study aims to assess whether mortality risks vary for different causes of death according to the duration since diagnosis and age in a large sample of patients with nonaffective psychotic disorder. METHODS: Data of patients with nonaffective psychotic disorder (n = 12,580) from 3 Dutch psychiatric registers were linked to the cause of death register of Statistics Netherlands and compared with personally matched controls (n = 124,143) from the population register. Death rates were analyzed by duration since the date of the registered diagnosis of the (matched) patient and their age using a Poisson model. RESULTS: Among patients, the rates of all-cause death decreased with longer illness duration. This was explained by lower suicide rates. For example, among those between 40 and 60 years of age, the rate ratios (RR) of suicide during 2-5 and > 5 years were 0.52 and 0.46 (p = 0.002), respectively, when compared with the early years after diagnosis. Compared with controls, patients experienced higher rates of natural death causes during all stages and in all age categories, rate ratios 2.35-5.04; p < 0.001-0.025. There was no increase in these rate ratios with increasing duration or increasing age for patients when compared with controls. CONCLUSIONS: The high risk of natural death causes among patients with nonaffective psychotic disorder is already present at a comparatively young age. This suggests caution in blaming antipsychotics or the accumulating effects of adverse lifestyle factors for premature death. It is better to proactively monitor and treat somatic problems from the earliest disease stages onward.

Testing the psychosis continuum: differential impact of genetic and nongenetic risk factors and comorbid psychopathology across the entire spectrum of psychosis.

A growing number of studies demonstrate high rates of subthreshold psychotic experiences, but there is considerable heterogeneity in rates due to study cohort and design factors, obscuring how prevalent psychotic experiences may or may not relate to rare psychotic disorders. In a representative general population sample (n = 4011) in Izmir, Turkey, the full spectrum of expression of psychosis was categorized across 5 groups representing (1) absence of psychosis, (2) subclinical psychotic experiences, (3) low-impact psychotic symptoms, (4) high-impact psychotic symptoms, and (5) full-blown clinical psychotic disorder and analyzed for continuity and discontinuity in relation to (1) other symptom dimensions associated with psychotic disorder and (2) proxies of genetic and nongenetic etiology. Results were tested for linear and extralinear contrasts between clinical and nonclinical and between disorder and nondisorder expression of psychosis. Demographic variables, indexing premorbid social adjustment and socioeconomic status, impacted mostly linearly; proxy variables of genetic loading (more or more severely affected relatives) impacted in a positive extralinear fashion; environmental risk factors sometimes impacted linearly (urbanicity and childhood adversity) and sometimes extralinearly (cannabis), occasioning a disproportional shift in risk at the clinical disorder end of the spectrum. Affective symptoms were associated with a disproportionally higher risk below the disorder threshold, whereas a disproportionally higher risk above the threshold was associated with psychotic symptom load, negative symptoms, disorganization, and visible signs of mental illness. Liability associated with respectively affective and nonaffective symptom domains, in interaction with environmental risks, may operate by impacting differentially over a quasi-continuous extended psychosis phenotype in the population.

Reduced cortical thickness as an outcome of differential sensitivity to environmental risks in schizophrenia.

BACKGROUND: The etiology of schizophrenia is thought to involve differential-likely genetically mediated-sensitivity to environmental exposures. However, examination of differential sensitivity in models of psychopathologic constructs is subject to bias because psychopathology itself may distort exposure assessment. The use of neuroimaging phenotypes, conversely, may provide unbiased evidence for differential sensitivity to environmental exposures. This study examined the impact of two environmental exposures associated with both schizophrenia and magnetic resonance imaging (MRI) cerebral alterations in models of cerebral cortical thickness. METHODS: T1-weighted MRI scans were acquired from 88 patients with schizophrenia, 98 healthy siblings at higher than average genetic risk for schizophrenia, and 87 control subjects. Freesurfer software was used to measure cortical thickness for 68 brain regions. Associations between 1) cortical thickness and 2) cannabis use and developmental trauma were examined. RESULTS: A significant group × developmental trauma interaction (χ(2) = 9.65, p = .01), as well as a significant group × cannabis interaction (χ(2) = 6.04, p = .05) was apparent, indicating differential sensitivity of the patient group, which displayed stronger reductions of cortical thickness for both exposures. A similar pattern was found in the sibling-control comparison for cannabis. For developmental trauma, siblings did not differ from control subjects, displaying an increase in cortical thickness with higher levels of trauma. CONCLUSIONS: The findings suggest that schizophrenia and its genetic liability are associated with differential cerebral cortical sensitivity to developmental environmental exposures such as cannabis. Gene-environment interactions may underlie some of the brain alterations observed in patients with schizophrenia and their relatives.

COMT Val158Met-stress interaction in psychosis: role of background psychosis risk.

BACKGROUND: The interplay between the catechol-O-methyltransferase (COMT) Val158Met polymorphism and environmental stress may have etiological relevance for psychosis, but differential effects have been reported in healthy control and patient groups, suggesting that COMT Val158Met interactions with stress may be conditional on background genetic risk for psychotic disorder. METHODS: Patients with a nonaffective psychotic disorder (n = 86) and control participants (n = 109) were studied with the experience sampling method (a structured diary technique) in order to assess stress, negative affect and momentary psychotic symptoms in the flow of daily life. RESULTS: Multilevel analyses revealed significant three-way interactions between group status (patient or control), COMT genotype and stress in the model of negative affect (χ(2)(2) = 13.26, P < 0.01) as well as in the model of momentary psychotic symptoms (χ(2)(2) = 6.92, P < 0.05). Exploration of the three-way interaction revealed that in patients, COMT genotype moderated the association between stress and negative affect (χ(2)(4) = 11.50, P < 0.005), as well as the association between stress and momentary psychosis (χ(2)(4) = 12.79, P < 0.005). Met/Met genotype patients showed significantly increased psychotic and affective reactivity to stress in comparison to the Val/Met and Val/Val genotypes. In contrast, healthy controls did not display large or significant COMT Val158Met X stress interactions. CONCLUSIONS: Important differences exist in the effect of COMT Val158Met on stress reactivity, which may depend on background risk for psychotic disorder. Differential sensitivity to environmental stress occasioned by COMT Val158Met may be contingent on higher order interactions with genetic variation underlying psychotic disorder.

No ecological effect modification of the association between negative life experiences and later psychopathology in adolescence: A longitudinal community study in adolescents.

BACKGROUND: The aim of the study was to examine the potential contribution of exposure to bullying and adverse life events to the development of psychopathology in adolescents, and possible effect modification by neighbourhood social capital. METHODS: Two waves of routine, longitudinal, standard health examinations at local community paediatric health services, pertaining to 749 adolescents living in Maastricht (The Netherlands) who were attending second grade of secondary school (age 13/14 years) and approximately 2 years later going to the fourth grade (age 15/16 years), were analysed. A self-report questionnaire was used, including measures of psychopathology and two measures of negative life experiences, exposure to bullying and adverse life events, that were available for both age groups and subjected to (multilevel) regression analysis. RESULTS: Exposure to bullying in the past school-year as well as the experience of adverse life events over a 12 month period, at the age of 13/14 years, predicted an increase in psychopathology at follow-up. Exposure to bullying was associated with the development of hyperactivity and emotional problems, while the experience of adverse life events predicted the development of conduct problems. Family-related adverse events had greatest effect sizes. Effects of bullying and adverse life events were not moderated by neighbourhood social capital. CONCLUSION: Negative life experiences impact on liability to psychopathology in adolescents independent of the wider social environment.

Childhood victimisation and developmental expression of non-clinical delusional ideation and hallucinatory experiences: victimisation and non-clinical psychotic experiences.

BACKGROUND: Victimisation in childhood may be associated with adult psychosis. The current study examined this association in the crucial developmental period of early adolescence and investigated whether (1) unwanted sexual experiences, and (2) being bullied, were associated with non-clinical delusional ideation and hallucinatory experiences in a general population sample of 14 year olds. METHODS: Data were derived from standard health screenings of the Youth Health Care Divisions of the Municipal Health Services in Maastricht, the Netherlands. A self-report questionnaire was filled out by a total of 1290 adolescents to assess non-clinical psychotic experiences, as well as experiences of being bullied and sexual trauma. RESULTS: Non-clinical psychotic experiences were strongly and independently associated with both bullying (OR=2.9, 95% CI 1.8-4.8) and sexual trauma (OR=4.8, 95% CI 2.3-10.1). CONCLUSIONS: The results suggest that reported associations between childhood victimisation and adult psychosis can be understood in a developmental framework of onset of at-risk mental states in early adolescence. In addition, the data suggest that the traumatic experience of being bullied may also feed the cognitive and biological mechanisms underlying formation of psychotic ideation.