Cannon M, Caspi A, Moffitt TE, et al. Evidence for early-childhood, pan-developmental impairment specific to schizophreniform disorder: results from a longitudinal birth cohort

University of Wisconsin–Madison, Madison, Wisconsin, United States
Archives of General Psychiatry (Impact Factor: 14.48). 06/2002; 59(5):449-56. DOI: 10.1001/archpsyc.59.5.449
Source: PubMed


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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    • "Higher risk of PE in early adolescence has been reported in individuals with childhood neurodevelopmental non-psychotic disorder (ND) (Khandaker et al. 2014), which is also a frequent co-morbid disorder (Jeppesen et al. 2015a). Lower intelligence quotient (IQ) is associated with schizophrenia (Woodberry et al. 2008; Khandaker et al. 2011) and may also be associated with PE in both non-clinical adult (Cannon et al. 2002; Johns et al. 2004) and child populations (Horwood et al. 2008; Polanczyk et al. 2010). However, these risk factors are to a large extent non-specific, and evidence supporting predictions as to which vulnerable individuals will develop which cluster of mental symptoms is sparse (Kounali et al. 2014). "
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    ABSTRACT: Background: Knowledge on the risk mechanisms of psychotic experiences (PE) is still limited. The aim of this population-based study was to explore developmental markers of PE with a particular focus on the specificity of hyper-theory-of-mind (HyperToM) as correlate of PE as opposed to correlate of any mental disorder. Method: We assessed 1630 children from the Copenhagen Child Cohort 2000 regarding PE and HyperToM at the follow-up at 11-12 years. Mental disorders were diagnosed by clinical ratings based on standardized parent-, teacher- and self-reported psychopathology. Logistic regression analyses were performed to test the correlates of PE and HyperToM, and the specificity of correlates of PE v. correlates of any Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) mental disorder. Results: Univariate analyses showed the following correlates of PE: familial psychiatric liability; parental mental illness during early child development; change in family composition; low family income; regulatory problems in infancy; onset of puberty; bullying; concurrent mental disorder; and HyperToM. When estimating the adjusted effects, only low family income, concurrent mental disorder, bullying and HyperToM remained significantly associated with PE. Further analyses of the specificity of these correlates with regard to outcome revealed that HyperToM was the only variable specifically associated with PE without concurrent mental disorder. Finally, HyperToM did not share any of the investigated precursors with PE. Conclusions: HyperToM may have a specific role in the risk trajectories of PE, being specifically associated with PE in preadolescent children, independently of other family and child risk factors associated with PE and overall psychopathology at this age.
    Psychological Medicine 09/2015; DOI:10.1017/S0033291715001567 · 5.94 Impact Factor
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    • "The continuum of psychosis does not concern only the phenomenological similarities between the experiences laying on its extremes, but they were also associated with similar risk factors, and similar cognitive [10] [11] [12] [13] [14], emotional [15] [16] and personality traits [17] [18] [19] [20] as the clinically relevant psychotic symptoms. What is more, the recent researches showed that the psychotic – like experiences may have similar neural correlates as psychotic disorders. "

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    • "While current antipsychotics ameliorate psychosis in schizophrenic patients, their effect on cognitive symptoms is only moderate at best [2]. The latter, however, precede the onset of psychosis [3], are present in non-affected relatives of schizophrenic patients [4] and are the best predictor of functional outcome [5], thus representing the core clinical feature of schizophrenia. It is believed that a combination of genetic or early environmental risk factors (e.g. "
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    ABSTRACT: Cognitive deficits are a particularly debilitating symptom group in schizophrenia. We investigated the effect of a 'two hit' combination of two factors implicated in schizophrenia development, reelin deficiency and stress, on cognitive behaviours in mice. Male and female heterozygous reelin mice (HRM) and wild-type (WT) controls received the stress hormone, corticosterone (CORT), during early adulthood to simulate chronic stress. The Y-maze, novel object recognition task (NORT), social interaction task and prepulse inhibition (PPI) were used to assess short-term spatial memory, visual non-spatial memory, social recognition memory and sensory gating, respectively. Reelin protein expression was measured in the prefrontal cortex (PFC) and hippocampus. CORT induced spatial memory deficits in male and female HRM but not in WT controls suggesting increased vulnerability of HRM to the effects of stress on cognition. By contrast, CORT disrupted PPI only in male WT mice, but not in male HRM, suggesting a protective role of reelin deficiency against effects of stress on PPI. Male HRM performed worse in the social recognition memory task compared to wild-type controls, irrespective of CORT treatment. No differences were detected in the NORT. Reelin protein expression was increased in the PFC of female CORT-treated HRM but there were no group differences in the hippocampus. Overall, these findings extend our understanding of the role of reelin-stress interactions in schizophrenia. Copyright © 2015. Published by Elsevier B.V.
    Behavioural brain research 04/2015; 287. DOI:10.1016/j.bbr.2015.03.063 · 3.03 Impact Factor
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