Community screening for psychotic-like experiences and other putative antecedents of schizophrenia in children aged 9-12 years

Department of Forensic Mental Health Science, Institute of Psychiatry, King's College London, Box P023, De Crespigny Park, London SE5 8AF, UK.
Schizophrenia Research (Impact Factor: 4.43). 03/2007; 90(1-3):130-46. DOI: 10.1016/j.schres.2006.11.006
Source: PubMed

ABSTRACT Prospective longitudinal investigations are needed to identify causal processes leading to schizophrenia. However, there is presently no cost-effective way to identify children who are at risk of developing schizophrenia spectrum disorders: Although having a family history of schizophrenia is associated with elevated risk for developing spectrum disorders, the majority of individuals with schizophrenia do not have an afflicted relative. The present study aimed to test the feasibility of screening a community sample of children, aged 9 to 12 years, to identify children who experienced a triad of putative antecedents of schizophrenia that had been identified from previous research, including: (1) speech and/or motor development lags or problems; (2) social, emotional, or behavioural problems; and (3) psychotic-like-experiences (PLEs). 548 children and 264 caregivers completed questionnaires. 9.2% of boys and 4.1% of girls displayed the triad of antecedents. 58.9% of the children reported "certain experience" of one or more PLEs. The results suggest that questionnaire screening of community samples of children for the putative antecedents of schizophrenia spectrum disorders is feasible. Accuracy of identification will only be established by follow-up studies.

Download full-text


Available from: Hodgins Sheilagh, Aug 30, 2015
  • Source
    • "Briefly, children aged 9–12 years and their caregivers independently completed questionnaires, at school and at home, respectively, assessing a triad of antecedents of schizophrenia, including: (i) a speech and/or motor delay or abnormality ; (ii) a social, emotional and/or behavioural problem; and (iii) a psychotic-like experience. Delays or abnormalities in speech and/or motor development were assessed via nine items included in the caregiver questionnaire (Laurens et al. 2007). Social, emotional and behavioural problems were defined as a score in the clinical range on at least one of the four psychopathology scales of the Strengths and Difficulties Questionnaire (SDQ; Goodman, 2001): emotional symptoms (childreported ); conduct problems; hyperactivity–inattention; and peer relationship problems (caregiver-reported). Psychotic-like experiences were assessed via nine items in the child questionnaire (Laurens et al. 2012); each item was rated on a three-point scale (0 = not true, 1 = somewhat true, 2 = certainly true) with a score of 2 on any item indicating a positive rating. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Pituitary volume enlargements have been observed among individuals with first-episode psychosis. These abnormalities are suggestive of hypothalamic-pituitary-adrenal (HPA) axis hyperactivity, which may contribute to the development of psychosis. However, the extent to which these abnormalities characterize individuals at elevated risk for schizophrenia prior to illness onset is currently unclear, as volume increases, decreases and no volume differences have all been reported relative to controls. The current study aimed to determine whether antipsychotic-naive, putatively at-risk children who present multiple antecedents of schizophrenia (ASz) or a family history of illness (FHx) show pituitary volume abnormalities relative to typically developing (TD) children. An additional aim was to explore the association between pituitary volume and experiences of psychosocial stress. ASz (n = 30), FHx (n = 22) and TD (n = 32) children were identified at age 9-12 years using a novel community-screening procedure or as relatives of individuals with schizophrenia. Measures of pituitary volume and psychosocial stress were obtained at age 11-14 years. Neither ASz nor FHx children showed differences in pituitary volume relative to TD children. Among FHx children only, pituitary volume was negatively associated with current distress relating to negative life events and exposure to physical punishment. The lack of pituitary volume abnormalities among ASz and FHx children is consistent with our previous work demonstrating that these children are not characterized by elevated diurnal cortisol levels. The findings imply that these biological markers of HPA axis hyperactivity, observed in some older samples of high-risk individuals, may emerge later, more proximally to disease onset.
    Psychological Medicine 07/2015; DOI:10.1017/S0033291715001282 · 5.43 Impact Factor
  • Source
    • "Recruitment of ASz and TD children: Children from 73 primary schools in greater London and their primary caregivers completed questionnaires designed to assess replicated antecedents of schizophrenia that have been described previously (Laurens et al., 2007, 2011). Children presenting antecedents of schizophrenia (ASz) met three criteria: (1) a child-reported " certainly-true " response on at least one of nine PLE items assessing hallucinationand delusion-like experiences (Laurens et al., 2012); (2) a score in the clinical range (approximately top tenth percentile of U.K. population norms) on the child-reported emotional symptoms scale or the caregiver-reported conduct problems, hyperactivityinattention , or peer relationship problems scales of the Strengths and Difficulties Questionnaire (Goodman, 2001); and (3) a caregiver-report of a delay/abnormality in motor and/or speech development (Laurens et al., 2007). In contrast, TD children were defined as those who presented none of the three ASz criteria nor had a first-, second-, or third-degree relative with a schizophrenia spectrum disorder, as confirmed using the Family Interview for Genetic Studies which was completed with the child's primary caregiver (FIGS: Maxwell, 1992). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Adults with schizophrenia present cognitive impairments, as do individuals at ultra-high risk for the disorder, youth with relatives with schizophrenia spectrum disorders, and children with antecedents of schizophrenia. The present study aimed to determine if impairments in childhood differed depending on the definition of risk and/or on the degree of relatedness to an affected individual, and if impairments were explained by IQ. Four groups of children aged 9-12 years were studied: (1) 13 children with ≥1 first-degree or ≥2 second-degree affected relatives (high familial loading: FHx(H)); (2) 14 with ≥1 affected second-degree relative (lower familial loading: FHx(L)); (3) 32 with well-replicated antecedents of schizophrenia (ASz); and (4) 45 typically-developing (TD) children with neither a positive family history nor antecedents. Compared to TD children, both FHx(H) and ASz children exhibited significantly poorer verbal comprehension, scholastic achievement, and verbal working memory, while FHx(H) children additionally displayed significantly lower full-scale IQ, and verbal memory and executive function impairments. After adjusting statistical analyses for IQ, group differences were attenuated. Relative to TD children, FHx(L) children showed no significant differences in performance. The results imply that impairments in verbal comprehension, scholastic achievement, and verbal working memory may index vulnerability for schizophrenia among children with affected relatives with the disorder and among those with multiple antecedents of the disorder who have no affected relatives. More accurate identification of children at-risk for schizophrenia and the specific deficits that they present provides opportunities for interventions such as cognitive remediation that may impact the development of the illness.
    Journal of Psychiatric Research 12/2013; 50. DOI:10.1016/j.jpsychires.2013.12.003 · 4.09 Impact Factor
  • Source
    • "Consequently, this chapter includes much speculation about both aetiological factors and neural mechanisms associated with aggressive behavior of these three phenotypes, but also proposed hypotheses that could be tested in future research. Prospective longitudinal studies following children characterised by known antecedents of schizophrenia (Cullen et al. 2012; Laurens et al. 2007, 2010) are needed to identify the mechanisms associated with aggressive behaviour in this population . Such studies offer the possibility of taking account of neural changes underlying transition to illness and the consequences on the brain and behaviour of both the changes and antipsychotic medication. "
    [Show abstract] [Hide abstract]
    ABSTRACT: People with schizophrenia are at increased risk, as compared to the general population, to acquire convictions for violent crimes and homicide. They also show elevated levels of aggressive behaviour. While psychotic symptoms explain aggressive behaviour that is common during acute episodes, they do not explain such behaviour at other stages of illness or prior to illness onset. Three distinct phenotypes have been identified: individuals with a childhood onset of conduct disorder who display antisocial and aggressive behaviour both before and after schizophrenia onset; individuals with no history of conduct problems who begin engaging in aggressive behaviour as illness onsets; and individuals who after many years of illness engage in a severe physical assault. Little is known about the aetiology aetiology of the three types of offenders and about the neural mechanisms that initiate and maintain these behaviours. We hypothesize that schizophrenia preceded by conduct disorder is associated with a combination of genes conferring vulnerability for both disorders and altering the effects of environmental factors on the brain, and thereby, with a distinct pattern of neural development. Some evidence is available to support this hypothesis. By contrast, offending among adults with schizophrenia schizophrenia who have no history of such behaviour prior to illness may result from the changes in the brain that occur as illness onsets, and that are further altered by comorbid conditions such as substance misuse, or by the progressive changes in the brain through adulthood that may result from the illness and from the use of antipsychotic medications.
    12/2013; 17. DOI:10.1007/7854_2013_259
Show more