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Childhood cognitive functioning in schizophrenia patients and their unaffected siblings: a prospective cohort study
T D Cannon1, C E Bearden, J M Hollister
1Department of Psychology, University of California, Los Angeles, 90095-1563, USA. cannon@psych.ucla.edu
Insights
Cognitive deficits in children with a parent diagnosed with schizophrenia are stable early indicators of vulnerability. These early cognitive impairments in preschizophrenia individuals are linked to genetic factors, not obstetric complications.
Area of Science:
- Neuroscience
- Psychiatry
- Developmental Psychology
Background:
- Children of parents with schizophrenia exhibit poorer cognitive functioning.
- Predictive value of early cognitive deficits for schizophrenia outcome is uncertain.
- Role of nongenetic factors in cognitive deficits requires clarification.
Purpose of the Study:
- To determine if early cognitive deficits predict schizophrenia.
- To investigate cognitive decline in preschizophrenia individuals during childhood.
- To assess the contribution of nongenetic factors to cognitive deficits.
Main Methods:
- Longitudinal study of a birth cohort with cognitive tests at ages 4 and 7.
- Ascertainment of adult psychiatric morbidity through public health service utilization.
- Diagnosis via DSM-IV criteria based on medical record review.
Main Results:
- Schizophrenia patients and unaffected siblings performed worse than controls on cognitive tests at ages 4 and 7.
- Preschizophrenia cases and siblings were overrepresented in lower cognitive performance quartiles.
- No significant cognitive decline or link to obstetric complications was found.
Conclusions:
- Premorbid cognitive dysfunction in schizophrenia is a stable vulnerability indicator from ages 4-7.
- Findings suggest primarily genetic or shared environmental influences.
- Early cognitive deficits are not significantly impacted by obstetric complications.
Abstract:
While it is known that children of schizophrenia parents perform more poorly on tests of cognitive functioning than children of normal parents, less certain is the degree to which such deficits predict schizophrenia outcome, whether cognitive functioning deteriorates during childhood in preschizophrenia individuals, and whether nongenetic etiologic factors (such as obstetric complications) contribute to these deficits. In the present study, 72 patients with schizophrenia or schizoaffective disorder, 63 of their siblings not diagnosed with schizophrenia, and 7,941 controls with no diagnosis were ascertained from a birth cohort whose members had been evaluated with standardized tests of cognitive functioning at 4 and 7 years of age. Adult psychiatric morbidity was ascertained via a longitudinal treatment data base indexing regional public health service utilization, and diagnoses were made by review of all pertinent medical records according to DSM-IV criteria. Both the patients with schizophrenia and their unaffected siblings performed significantly worse than the nonpsychiatric controls (but did not differ from each other) on verbal and nonverbal cognitive tests at 4 and 7 years of age. Preschizophrenia cases and their siblings were increasingly overrepresented across decreasing quartiles of the performance distributions. There was not significant intra-individual decline, and there were no significant relationships between obstetric complications and test performance among the preschizophrenia subjects. These results suggest that during the period from age 4 to age 7 years, premorbid cognitive dysfunction in schizophrenia represents a relatively stable indicator of vulnerability deriving from primarily genetic (and/or shared environmental) etiologic influences.