Epidemiological research has shown that the majority of children who need professional mental health care do not receive it. Factors other than the level of the child's problem behaviour are involved in the help-seeking process, and are co-determinants of whether or not the child receives help. Longitudinal general population studies have shown that child psychopathology can persist and may lead to later serious adjustment problems, even in adult life. Consequently, it seems important that child psychologists and child psychiatrists should not wait passively until the patient steps into the office, but should actively trace high-risk children and apply the most effective intervention programmes. But how can children most in need of professional interventions be selected accurately? The central question addressed in the Annotation by Bennett et al. in this issue concerns externalising problems. The authors give an account of the most relevant epidemiological measures needed for the assessment of the predictive accuracy of externalising behaviours. They reviewed studies and tested the accuracy with which measures of externalising behaviours in children from the general population predict later antisocial behaviours. Selecting only those studies that pertained to kindergarten and grade one children, they came to the sobering conclusion that the predictive accuracy of externalising symptoms at that age has been overestimated and is, at best, modest. However, as they point out, targeted intervention programmes, in which high-risk children are selected, may still offer some advantages, because even with far from accurate predictive measures the number of children who receive unnecessary interventions can still be substantially reduced. The authors rightly note the risk of labelling due to false positive errors. They also claim that, when the same method is used to detect the presence of externalising behaviours in both females and males, a higher rate of false positive errors in females will occur, with a consequently greater risk for labelling for females. However, they seem to have overlooked that it is possible to select different morbidity or high-risk criteria for each sex separately; by using norm-based measures of problem behaviour, we can use the distributions of problem behaviours in the norm population for each sex separately to determine which cut-off separates high- from low-risk boys and girls. Even if we have improved our means to select accurately those children that run a high risk for later problems, we still have to determine which preventive intervention strategies work best, and who is going to treat all the high-risk children thus selected.

Mental health professionals involved with the care of children and adolescents are frequently confronted with questions about the risk of later troublesome outcomes. Of particular concern is whether the presence of certain risk factors warrants the provision of an intervention. The presence of externalising behaviour symptoms is regarded by many as the single best predictor of risk for future conduct disorder and antisocial behaviour (Loeber, 1991; Lynam, 1996; Moffitt, 1993; Patterson, 1993; Yoshikawa, 1994). These symptoms include aggression against others, destruction of the personal property of others, temper tantrums, and noncompliance, to name but a few. The evidence suggests that when these behaviours are present in childhood there is an increased risk for persistent, life-long psychosocial problems (Loeber, 1982; Loeber & Dishion, 1983; Moffitt, 1993; Olweus, 1979; Yoshikawa, 1994). For example, a link between the early onset of externalising behaviours and the later development of conduct disorder, antisocial behaviour, and substance abuse has been documented in both longitudinal and retrospective studies (Caspi, Moffitt, Newman, & Silva, 1996; Farrington, 1990; Robins, 1978; Tremblay, Pihl, Vitaro, & Dobkin, 1994; White, Moffitt, Earls, Robins, & Silva, 1990; Zoccolillo, Tremblay, & Vitaro, 1996).

The risks associated with externalising symptoms and the relatively modest effectiveness of treatment for established cases of conduct disorder and antisocial behaviour (Kazdin, 1997; Offord, 1989; Offord & Bennett, 1994) have led to an increased emphasis on the provision of preventive interventions (Institute of Medicine, 1994; Reiss & Price, 1996). It has been argued that intervention should be provided to high-risk children as early as possible. Claims have been made that even in nonclinic populations of children as young as 4 and 5 years of age, 50% or more of those with troublesome externalising symptoms will develop persistent psychosocial problems (Campbell, 1995; Coie, 1996; Reid, 1993; Reid & Patterson, 1991).

This paper reviews the management of schizophrenia occurring during childhood and adolescence. It considers the clinical features of the disorder particular to its early onset before providing a practical framework for assessment and treatment based upon a critical review of the available literature. A multi-modal approach to treatment encompassing the individual and their family is adopted with the roles of pharmacological, psychological, and environmental interventions all considered. The place of the newer “atypical” antipsychotic agents and the likelihood that they will soon become the first-line drugs of choice is particularly discussed.

The adjustment and prosocial behaviour of 4-year-old children and their older siblings growing up in step-parent or single-parent families, or with two biological parents, was investigated within a longitudinal community study, the Avon Longitudinal Study of Pregnancy and Childhood (ALSPAC). Mean differences in mothers' perception of adjustment were found for children in different family settings, with higher levels of problems and lower prosocial scores reported for those in single- and step-parent families than those in non-stepfamilies. Individual differences within each family setting were marked. With the exception of single parenthood, which remained a risk indicator for the 4-year-olds, the contribution of family type to differences in adjustment and prosocial behaviour largely disappeared when account was also taken of negativity in family relationships, maternal age, education level, depressive symptomatology, and history of previous live-in relationships, mothers' support networks, and the family's current financial and housing circumstances. Boys remained more at risk for adjustment difficulties than girls when this range of factors was taken into account. The limitations and implications of these findings on a community sample, a first step in a programme of research into family processes in children's adjustment, are discussed.

Associations between the extent of conduct problems at age 8 years and later life opportunity outcomes at age 18 years were examined in a birth cohort of New Zealand children studied prospectively to age 18 years. Conduct problems at age 8 were assessed using a combination of parent and teacher reports of conduct disordered and oppositional behaviours. Two measures of life opportunities were assessed at age 18: (a) whether the young person had left school by age 18 without educational qualifications; (b) whether the young person had experienced a period of unemployment of 3 months or longer following school leaving. The analysis suggested the following conclusions: (1) There were clear and significant (p<.0001) tendencies for increasing levels of conduct problems at age 8 to be associated with increasing risks of leaving school without qualifications and of unemployment by age 18. (2) A substantial component of these associations was explained by a series of confounding social, family, and individual factors (notably child intelligence, early attentional problems, and family sociodemographic disadvantage) that were associated with both early conduct problems and later life opportunities. (3) Further analysis suggested that linkages between early conduct problems and later educational underattainment and unemployment (after adjustment for confounders) were mediated by a series of adolescent behavioural processes including patterns of peer affiliations, substance use, truancy, and problems with school authority.

This study examined central inhibitory function in children with Tourette syndrome (TS; N=46) and normally developing controls (N=22) matched on age, gender, and IQ. A negative priming task measured the ability to inhibit processing of irrelevant distractor stimuli presented on a visual display. Initial analyses indicated that participants with Tourette syndrome did not differ significantly in inhibitory function from controls. However, when the large Tourette syndrome sample was separated into subgroups, one without evidence of comorbidity (N=23) and the other meeting research criteria for either AD/HD, OCD, or both (N=23), it became evident that individuals with Tourette syndrome with comorbid conditions tended to perform less well than the control group, whereas those without comorbidity performed much like controls. Similarly, when the large Tourette syndrome sample was divided into two subgroups on the basis of severity of symptomatology (N=23 in each), those with more numerous and severe symptoms of Tourette syndrome, AD/HD, and OCD performed significantly less well than both controls and Tourette syndrome subjects with fewer and less severe symptoms. This suggests that neuropsychological impairment occurs as a function of comorbidity and symptom severity in Tourette syndrome. It also suggests that categorical diagnoses alone may be less useful than dimensional methods for predicting cognitive impairment in individuals with Tourette syndrome.

Recent research suggests a significant relationship between verbal short-term memory and normal language development. Although poor short-term memory and impaired language are features of Down syndrome there has been little investigation of the relationship between these functions in this population, and no studies have included the nonword repetition test devised by Gathercole and Baddeley on which much of the evidence from normal development is based. This study reports the use of nonword repetition with 33 children and teenagers with Down syndrome aged from 5 to 18 years, and investigates the relationship between this test and other memory and language measures. Word repetition was included as an indirect control for the perceptual and speech impairments often associated with this group. Words were repeated significantly more successfully than nonwords and both these tasks were sensitive to word length. Nonword repetition was significantly correlated with age, and when age and nonverbal cognitive ability were controlled, nonword repetition was significantly correlated with all other language-based memory measures, i.e. auditory digit span, word span, sentence repetition, and fluency, and also with memory for a sequence of hand movements, but not with memory for faces or a visual digit span task. There was also a significant relationship between nonword repetition and receptive vocabulary, language comprehension, and reading. When performance on the word repetition task was controlled in addition to age and nonverbal ability, significant correlations between nonword repetition and word span, sentence memory, hand movements, language comprehension, and reading remained. Fewer relationships between auditory digit span and these other measures were established; in particular, there was no association between digit span and the language and reading measures. Results suggest that nonword repetition is a reliable measure of phonological memory in Down syndrome and can predict language comprehension and reading ability.

This study employed the self-understanding interview of Damon and Hart (1988) to assess the self-concepts of two groups of children and adolescents: a group of individuals with autism and a group of nonautistic mentally retarded individuals who were matched for age and for verbal ability. On the basis of an hypothesis concerning the interpersonal origins of social and psychological self-concepts (Hobson, 1990; Neisser, 1988), it was predicted that the participants with autism would show a relative dearth of such concepts in their talk about themselves. In accordance with our predictions, there was a significant group difference in the number and quality of statements that fell into the social category of self-concept; contrary to our predictions, however, there was no group difference in the number of statements that fell into the psychological category. In addition, although there were not significant group differences in the overall production of verbally expressed concepts concerning self-attributes of a physical, active, or psychological kind, even within these categories individuals with autism made fewer references to social interactions or qualities. These results are discussed with regard to theories of self-concept development in typically developing as well as autistic and mentally retarded individuals, and with reference to the limitations of interpersonal understanding (“theory of mind”) in people with autism.

This study examined spontaneous blink rate, a putative measure of dopamine function, in 30 children with complex partial epilepsy and 61 normal children. The children with epilepsy had significantly lower blink rates than the normal children in a conversation and a verbal recall task, particularly if they had a schizophrenia-like psychosis, EEG evidence for left focal epileptic activity, illogical thinking, discourse deficits, and distractibility. They modulated their blink rates across a listening, a conversation, and a verbal recall task like the normal children. Given previously reported low blink rates in schizophrenic children, these findings suggest that children with complex partial epilepsy or schizophrenia might have similar biological features.

A twin study design was used to examine to what extent genetic and environmental factors mediate the association between life events and depressive symptoms. Questionnaire measures (maternally rated) of depressive symptoms and life events were obtained for a systematically ascertained sample of 270 twin pairs aged 8 to 17 years. Bivariate genetic model fitting showed that depressive symptoms and some life events (total events, negative impact) share a common genetic influence. The covariation of independent life events and depressive symptoms was explained by a shared environmental influence common to both. At least part of the association between life events and depressive symptoms is mediated by familial factors that include both genes and shared environment.