Violence and aggression are relatively common and serious occurrences in health and social care and rates are higher in mental health settings. Despite the National Health Service's policy of ‘zero tolerance’ of such behaviour, reporting of violence and aggression against mental health staff remains low. This article considers the nature of violence and aggression against staff in psychiatric settings and the process of involving the police to ensure an effective outcome. It outlines each step, from the initial the multidisciplinary team assessment of the incident and its reporting to the police to the making of witness statements, should the case come to court. It also explains the discretionary role of the police in deciding whether to charge and of the Crown Prosecution Service (CPS) in deciding whether to prosecute. The article stresses that NHS organisations need to provide an effective, streamlined and time-efficient reporting process, as this should reduce levels of patient violence, improve staff's well-being and morale, save costs and make the working environment safer for all.

Several theoretical studies have suggested that large samples of randomly ascertained siblings can be efficiently used to ascertain phenotypically extreme individuals and increase power to detect genetic linkage. Phenotypes that can be reliably measured by questionnaire are of obvious utility for such selection strategies, as large numbers of individuals can be contacted without laborious individual interview. As the first step in developing a large randomly-ascertained family cohort in southwest England, a sample of 88 000 individuals, including more than 34 000 sibling pairs in 20 000 sibships, was administered the Eysenck Personality Questionnaire (EPQ) by commercial mailing. The sample age ranges were 20–67 years and comprised 59% males and 41% females. Descriptive properties of the EPQ scales are similar to those reported from other large family cohorts. Test–retest correlations on 1681 probands in the sample are substantial for the N-scale (r = 0.93), but somewhat more modest for the other scales (range r = 0.70–0.88). Phenotypic and sibling correlations correspond quite closely to those of twin studies. Twin Research (2000) 3, 310–315.

The idea that some phenotypes bear a closer relationship to the biological processes that give rise to psychiatric illness than diagnostic categories has attracted considerable interest. Much effort has been devoted to finding such endophenotypes, partly because it is believed that the genetic basis of endophenotypes will be easier to analyse than that of psychiatric disease. This belief depends in part on the assumption that the effect sizes of genetic loci contributing to endophenotypes are larger than those contributing to disease susceptibility, hence increasing the chance that genetic linkage and association tests will detect them. We examine this assumption by applying meta-analytical techniques to genetic association studies of endophenotypes. We find that the genetic effect sizes of the loci examined to date are no larger than those reported for other phenotypes. A review of the genetic architecture of traits in model organisms also provides no support for the view that the effect sizes of loci contributing to phenotypes closer to the biological basis of disease is any larger than those contributing to disease itself. While endophenotype measures may afford greater reliability, it should not be assumed that they will also demonstrate simpler genetic architecture.

We describe four children with dysmorphic syndrome with severe learning disability (SLD). Their chromosomes had been normal on conventional cytogenetic examination. However, screening using a multiprobe fluorescence in situ hybridisation (FISH) technique for subtelomeric abnormalities revealed a deletion of the p arm of chromosome 1. The physical features include body asymmetry, microcephaly, distinctive facies with deep-set eyes, sharply defined eye sockets, and mid-face hypoplasia; the neurodevelopmental profile was characterised by SLD, motor delay with hypotonia, markedly delayed visual maturation, and postural asymmetry together with epilepsy. This phenotype is consistent with that described for partial monosomy for 1p36.3.