The Antecedents of Schizophrenia: A Review of Birth Cohort Studies (original) (raw)
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Schizophrenia Research, 2008
Delayed neuromotor development carries an increased risk of developing schizophrenia, and some authors have assumed that risk factors for schizophrenia such as delayed development are also prognostic indicators for patients with established illness. In those who do develop schizophrenia, it is not clear if these same early developmental markers influence the outcome of illness. Our aim was to examine the association between infant developmental milestones and a range of outcomes in patients with schizophrenia. Our sample was drawn from Northern Finland 1966 Birth Cohort and included 109 subjects for whom prospectively collected information on age of learning to stand, walk and talk was available and who had developed schizophrenia by the age 35 years. By utilizing national registers we examined outcomes related to service utilization, educational achievement, and occupational status. Age of illness onset was also analyzed. Based on the diagnostic interview, a subgroup of 59 cases was assessed in clinical examinations on functioning and quality of life. Contrary to a widespread assumption within the field of schizophrenia research, later attainment of developmental milestones was not associated with poor outcome. We conclude that risk factors for schizophrenia are not necessarily prognostic factors.
Schizophrenia Research, 2010
The aim of the present study was to investigate the relationship between age of neuromotor milestone attainment and risk of adult schizophrenia. 5765 mothers of the Copenhagen Perinatal Cohort recorded 12 developmental milestones during the child's first year of life. Cohort members were followed until they were 46-48 years old through record linkage with the Danish Psychiatric Central Research Register. The age at which milestones were met in the 92 individuals who later developed schizophrenia was compared with milestone attainment in the 691 individuals who developed other psychiatric disorders and in the 4982 cohort controls who were never admitted to a psychiatric department. Group comparisons were adjusted for gender, mother's age, father's age, parental social status, breadwinner's education, single mother status and parity. Individuals who developed schizophrenia reached all developmental milestones later than controls and differed significantly from the controls with respect to the mean age of reaching the 12 milestones. Five developmental milestones in particular (smiling, lifting head, sitting, crawling, and walking) differed significantly. Individuals who later developed psychiatric disorders other than schizophrenia reached most developmental milestones earlier than those who developed schizophrenia, but later than the controls. The two psychiatric groups only differed significantly with respect to age of walking without support. The findings corroborate and methodologically extend previous research from prospective longitudinal cohort studies suggesting developmental delays observable as early as within the first year of life. These early developmental delays may not only characterize schizophrenia, but may be associated with a range of psychiatric disorders.
Schizophrenia Research, 2001
Delayed childhood development may precede adult psychoses. We tested this hypothesis in a large, general population birth cohort n 12 058 followed to age 31 years. The ages at which individuals learned to stand, walk, speak, and became pottytrained (bowel control) and dry (bladder control), were recorded at a 1-year examination. Psychiatric outcome was ascertained through linkage to a national hospital discharge register. Cumulative incidence of DSM-III-R schizophrenia, other psychoses and non-psychotic disorders were strati®ed according to the timing of milestones and compared within the cohort using internal standardization. 100 cases of DSM-III-R schizophrenia, 55 other psychoses, and 315 non-psychotic disorders were identi®ed. The ages at learning to stand, walk and become potty-trained were each related to subsequent incidence of schizophrenia and other psychoses. Compared with the whole cohort, earlier milestones reduced, and later milestones increased, the risk in a linear manner. These developmental effects were not seen for non-psychotic outcomes. The ®ndings support hypotheses regarding psychosis as having a developmental dimension with precursors apparent in early life. q
Schizophrenia Research, 2004
Childhood precursors of schizophrenia include multiple abnormalities of development. Continuities between early and subsequent deviance are poorly characterised. We studied associations among premorbid developmental deviance using data at ages 1 year (learning to stand, walk, and speak, attainment of bladder and bowel control) and 16 years (success at school). Generalised linear modelling was used to examine differential linear associations and trends across adult psychiatric diagnoses. In babies who, as adults, suffered schizophrenia or any psychosis, those who learned to stand latest were also more likely to perform poorly at school in both motor and theoretical domains at age 16 when compared with earlier learners. The effect was independent of genetic and perinatal factors. We conclude that the early developmental deviation in the first year of life is associated with lower school performance at age 16. Developmental continuity among children who develop psychoses was stronger than among normal controls and those hospitalised for non-psychotic psychiatric disorder. These findings are in line with hypothesis that a neural diathesis is present during postnatal brain development before schizophrenia. This supports the longitudinal dimension and life span models of schizophrenia.
European Psychiatry, 2015
BackgroundDelayed motor development in infancy and family history of psychosis are both associated with increased risk of schizophrenia, but their interaction is largely unstudied.AimTo investigate the association of the age of achieving motor milestones and parental psychosis and their interaction in respect to risk of schizophrenia.MethodsWe used data from the general population-based prospective Northern Finland Birth Cohort 1966 (n = 10,283). Developmental information of the cohort members was gathered during regular visits to Finnish child welfare clinics. Several registers were used to determine the diagnosis of schizophrenia among the cohort members and psychosis among the parents. Altogether 152 (1.5%) individuals had schizophrenia by the age of 46 years, with 23 (15.1%) of them having a parent with psychosis. Cox regression analysis was used in analyses.ResultsParental psychosis was associated (P < 0.05) with later achievement of holding the head up, grabbing an object, ...
Risk factors for schizophrenia. Follow-up data from the Northern Finland 1966 Birth Cohort Study
World psychiatry : official journal of the World Psychiatric Association (WPA), 2006
This paper updates single risk factors identified by the Northern Finland 1966 Birth Cohort Study up to the end of year 2001 or age 34. Impaired performance (e.g., delayed motor or intellectual development) or adverse exposures (e.g., pregnancy and birth complications, central nervous system diseases) are associated with an increased risk for schizophrenia. However, upper social class girls and clever schoolboys also have an increased risk to develop schizophrenia, contrasted to their peers. Individuals who subsequently develop schizophrenia follow a developmental trajectory that partly and subtly differs from that of the general population; this trajectory lacks flexibility and responsiveness compared to control subjects, at least in the early stages. We propose a descriptive, lifespan, multilevel systems model on the development and course of schizophrenia.
Schizophrenia Bulletin, 2000
The present study uses data from the Prenatal Determinants of Schizophrenia (PDS) Study to derive age-and sex-specific estimates of incidence and cumulative risk for DSM-FV schizophrenia. Although not designed as an incidence study, the PDS Study uses both a well-defined population under continuous followup and DSM-IV diagnoses. The originating cohort was established in Alameda County, California, during 1959-1967 and yielded 12,094 cohort members followed from 1981 to 1997 during the principal ages at risk for schizophrenia. Survival analytic techniques showed that schizophrenia incidence rates per 10,000 person-years for men were 9.4 for ages 15-19; 5.6 for ages 20-24; 33 for ages 25-29; and 0.9 for ages 30-34. Schizophrenia incidence rates per 10,000 person-years for women were 1.6 for ages 15-19; 13 for ages 20-24; and 4.1 for ages 25-29. The cumulative risk for schizophrenia by age 38 was 0.93 percent for men and 035 percent for women. These estimates of incidence rates and risk were higher than those in traditional incidence studies but similar to recent Findings in other cohorts. Possible explanations for the apparently high rates of disorder include chance, design effects, and true variation in risk over time and place.
The Design of the Prenatal Determinants of Schizophrenia Study
Schizophrenia Bulletin, 2000
This paper describes the Prenatal Determinants of Schizophrenia (PDS) Study; three companion papers report the first results. The PDS Study was designed to study early antecedents of schizophrenia in a birth cohort of 1959-1967 for whom a wealth of archived prenatal data-including maternal sera-was available. Making use of the registries of a health plan into which the cohort was born, we ascertained and then diagnosed 71 cases of schizophrenia and spectrum disorders in the cohort We describe herein the available prenatal data, the process of case diagnosis, and the strategies used to analyze prenatal determinants of schizophrenia in this cohort. Data are presented that bear on the main sources of potential bias and are important to understanding the strengths and limitations of this unique data set.
Journal of Psychiatric Research, 1996
Recently McNeil et al. (1993b), showed that schizophrenics had smaller head circumference (HC) at birth than controls. This small head size at birth was observed more commonly among schizophrenics without a family history of psychosis than among familial schizophrenics, suggesting that some prenatal environmental factors, rather than genetic factors, are related to the impaired brain growth in utero. We attempted to replicate this finding in 100 Japanese schizophrenics (DSM-III-R), using contemporaneous data on body measures at birth. Conversely, in the current study, HC at birth was found to be significantly smaller in schizophrenics with a family history of psychosis (N = 19) than those without (N = 81). A multiple regression analysis, controlling for gender, gestational age, maternal age, birth order and year of birth, yielded an overall reduction of about I cm in HC at birth among familial schizophrenics compared with non-familial schizophrenics. When HC at birth in family history positive and negative groups was compared separately with the local population norms with adjustment for gender and gestational age, familial and non-familial schizophrenics were both found to have significantly smaller HC at birth, although the difference was less marked for the latter. These results suggest that schizophrenics have delayed cerebral development in utero, and that genes which operate on prenatal neurodevelopment may play an important role in the aetiology of schizophrenia, although it is possible that some environmental factors may also be involved in the impaired brain growth.