Evidence for early-childhood, pan-developmental impairment specific to schizophreniform disorder - Results from a longitudinal birth cohort
ABSTRACT Childhood developmental abnormalities have been previously described in schizophrenia. It is not known, however, whether childhood developmental impairment is specific to schizophrenia or is merely a marker for a range of psychiatric outcomes.
A 1-year birth cohort (1972-1973) of 1037 children enrolled in the Dunedin Multidisciplinary Health and Development Study was assessed at biennial intervals between ages 3 and 11 years on emotional, behavioral, and interpersonal problems, motor and language development, and intelligence. At age 11 years, children were asked about psychotic symptoms. At age 26 years, DSM-IV diagnoses were made using the Diagnostic Interview Schedule. Study members having schizophreniform disorder (n = 36 [3.7%]) were compared with healthy controls and also with groups diagnosed as having mania (n = 20 [2%]) and nonpsychotic anxiety or depression disorders (n = 278 [28.5%]) on childhood variables.
Emotional problems and interpersonal difficulties were noted in children who later fulfilled diagnostic criteria for any of the adult psychiatric outcomes assessed. However, significant impairments in neuromotor, receptive language, and cognitive development were additionally present only among children later diagnosed as having schizophreniform disorder. Developmental impairments also predicted self-reported psychotic symptoms at age 11 years. These impairments were independent of the effects of socioeconomic, obstetric, and maternal factors.
The results provide evidence for an early-childhood, persistent, pan-developmental impairment that is specifically associated with schizophreniform disorder and that predicts psychotic symptoms in childhood and adulthood.
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ABSTRACT: Although we have studied schizophrenia as a major disease entity over the past century, its causes and pathogenesis remain obscure. In this article, we critically review genetic and other epidemiological findings and discuss the insights they provide into the causes of schizophrenia. The annual incidence of schizophrenia averages 15 per 100,000, the point prevalence averages approximately 4.5 per population of 1000, and the risk of developing the illness over one's lifetime averages 0.7%. Schizophrenia runs in families and there are significant variations in the incidence of schizophrenia, with urbanicity, male gender, and a history of migration being associated with a higher risk for developing the illness. Genetic factors and gene-environment interactions together contribute over 80% of the liability for developing schizophrenia and a number of chromosomal regions and genes have been "linked" to the risk for developing the disease. Despite intensive research and spectacular advances in molecular biology, however, no single gene variation has been consistently associated with a greater likelihood of developing the illness and the precise nature of the genetic contribution remains obscure at this time. Environmental factors linked to a higher likelihood of developing schizophrenia include cannabis use, prenatal infection or malnutrition, perinatal complications, and a history of winter birth; the exact relevance or nature of these contributions is, however, unclear. How various genetic and environmental factors interact to cause schizophrenia and via which precise neurobiological mechanisms they mediate this effect is not understood. Etiological heterogeneity, complex patterns of gene-gene and gene-environment interaction, and inadequately elucidated schizophrenia pathophysiology are among the explanations invoked to explain our inadequate understanding of the etio-pathogenesis of schizophrenia. The ability to question some of our basic assumptions about the etiology and nature of schizophrenia and greater rigor in its study appear critical to improving our understanding about its causation.Schizophrenia Research 08/2008; 102(1-3):1-18. DOI:10.1016/j.schres.2008.04.011 · 4.43 Impact Factor
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ABSTRACT: Schizophrenia is associated with severe deficits in social functioning. Similar deficits may be present prior to psychosis onset, in childhood and adolescence. If so, then prepsychosis social deficits could provide clues to the development of pathological processes in preschizophrenia children and could potentially improve early identification of the disorder and suggest targets for intervention. Evidence is reviewed from birth cohort, case- control, and familial high-risk studies within distinct periods of development to clarify the nature, timing, and specificity of social deficits in preschizophrenia children and adolescents. The results indicate that poor social functioning does differentiate preschizophrenia children and adolescents from their peers and can be a sensitive and potentially specific predictor of schizophrenia, not just psychopathology in general. Furthermore, age (but not sex) appears to be an important moderator of the strength and specificity of the association between particular social deficits (e.g., externalizing, internalizing) and later schizophrenia. Results are discussed in the context of current developmental theories of timing and pathophysiology of schizophrenia involving hypothalamic- pituitary-adrenal dysregulation. Implications for the early identification and treatment of preschizophrenia individuals are also considered.Psychological Bulletin 08/2008; 134(4):561-83. DOI:10.1037/0033-2909.34.4.561 · 14.39 Impact Factor
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ABSTRACT: Birth cohort studies have shown that individuals who develop non-affective psychoses display subtle deviations in behaviour during childhood and adolescence. We had the opportunity to examine the widely used Child Behavior Checklist (CBCL) and the Youth Self-Report (YSR) to explore the antecedents of non-affective psychosis. Based on a birth cohort of 3801 young adults, psychopathology was assessed at years 5 and 14 using the CBCL and/or the YSR. Screen-positive non-affective psychosis (SP-NAP) was assessed at year 21 by using the Composite International Diagnostic Interview (CIDI) or a self-report checklist. The association between childhood symptoms and SP-NAP was examined using logistic regression. Of the cohort, 60 subjects were classified as SP-NAP. In males, SP-NAP was associated with higher scores: (a) on year 5 CBCL 'Total', 'Aggression' and 'Social, Attention and Thought' scores; (b) on year 14 CBCL 'Social', 'Attention' and 'Delinquency' scores, and (c) YSR 'Total' and many YSR subscores. These associations were less clear for females. Hallucinations at year 14 were associated with SP-NAP for both sexes. Boys with high 'Total' scores at both years 5 and 14 were at greatest risk of SP-NAP (a 5-fold risk), followed by boys and girls whose 'Social, Attention and Thought' scores either increased or remained high from years 5 to 14 (3- to 13-fold risk). Individuals who screen positive for non-affective psychosis show increased psychopathology during childhood and adolescence. The psychopathological trajectory of children who go on to develop schizophrenia anticipates the heterogeneity associated with the full clinical syndrome.Psychological Medicine 08/2008; 39(4):625-34. DOI:10.1017/S0033291708003760 · 5.43 Impact Factor