AIM To assess the frequency, pervasiveness, associated features, and persistence of emotional and behavioural problems in a community sample of young children with autism spectrum disorder (ASD).METHOD Parents (n=277) and teachers (n=228) of 4-to 8-year-olds completed the Developmental Behaviour Checklist (DBC). Intellectual ability and autism symptomatology were also assessed. A subsample repeated the DBC.RESULTS Three-quarters of the cohort scored above the clinical cut-off on the Developmental Behaviour Checklist Primary Carer Version (DBC-P) questionnaire; almost two-thirds of these scored above cut-off on the Developmental Behaviour Checklist Teacher Version (DBC-T) questionnaire. In 81%, problems persisted above threshold 14 months later. Higher DBC-P scores were associated with greater autism symptomatology, higher deprivation index, parental unemployment, and more children in the home but not with parental education or ethnicity, or child's age or sex. Children with IQ>70 scored higher for disruptive behaviour, depression, and anxiety symptoms; those with IQ<70 scored higher for self-absorption and hyperactivity. INTERPRETATIONThe DBC identifies a range of additional behaviour problems that are common in ASD and which could be the focus for specific intervention. The results highlight the potential benefit of systematic screening for co-existing problems.Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impairments in reciprocal social interaction, communication, and repetitive, stereotyped interests and behaviours. 1 Recent estimates suggest a prevalence rate of over 1%. 2 ASD is associated with high comorbidity and significant costs to individuals, families, and services. 3 Emotional and behavioural problems in ASD are frequent, 4 and rates of social anxiety, attentiondeficit-hyperactivity disorder and oppositional disorder are elevated compared both with the general population 5 and with children with intellectual disability. [6][7][8] Functional problems in sleeping, eating, and toileting are also increased. High rates of behavioural and emotional disturbance are evident from pre-school onwards 9 and many children have two or more comorbid problems. 10,11 In non-ASD populations with and without intellectual disability, prevalence and types of emotional and behavioural difficulties are associated with age, sex, IQ, ethnic group, and social disadvantage. 5,7 In ASD these factors are less clearly linked to psychiatric co-morbidity 6,11 although the type of difficulty does vary with IQ, age, and sex. 6 Psychiatric disorders also have a high prevalence in adults 12 and, together with functional problems, can have as great an adverse impact as core ASD symptoms. There is, nevertheless, a range of evidence-based interventions that could reduce the effects of these problems. 13 Hence systematic assessment of emotional/behavioural difficulties by clinicians is crucial. This paper describes the use of parent and teacher questionnaires to assess comorbid emotional and behavioural ...

Optimal dosing of methylphenidate is practical and effective in some children with hyperkinetic disorder and intellectual disability. Adverse effects typical of methylphenidate were seen and medication use may require close monitoring in this vulnerable group.

Many diseases caused by trinucleotide expansion exhibit increased severity and decreased age of onset (genetic anticipation) in successive generations. Apparent evidence of genetic anticipation in schizophrenia has led to a search for trinucleotide repeat expansions. We have used several techniques, including Southern blot hybridization, repeat expansion detection (RED) and locus-specific PCR to search for expanded CAG/CTG repeats in 12 families from the United Kingdom and 11 from Iceland that are multiplex for schizophrenia and demonstrate anticipation. The unstable DNA theory could also explain discordance of phenotype for schizophrenia in pairs of monozygotic twins, where the affected twin has a greater number of repeats than the unaffected twin. We used these techniques to look for evidence of different CAG/CTG repeat size in 27 pairs of monozygotic twins who are either concordant or discordant for schizophrenia. We have found no evidence of an increase in CAG/CTG repeat size for affected members in the families, or for the affected twins in the MZ twin sample. Southern hybridization and RED analysis were also performed for the twin and family samples to look for evidence of expansion of GAA/TTC repeats. However, no evidence of expansion was found in either sample. Whilst these results suggest that these repeats are not involved in the etiology of schizophrenia, the techniques used for detecting repeat expansions have limits to their sensitivity. The involvement of other trinucleotide repeats or other expandable repeat sequences cannot be ruled out.

No abstract