The origins of cognitive deficits in victimized children : implications for neuroscientists and clinicians Andrea Danese, Terrie E. Moffitt, Louise Arseneault, Ben A. Bleiberg, Perry B. Dinardo, Stephanie B. Gandelman, Renate Houts, Antony Ambler, Helen L. Fisher, Richie Poulton, Avshalom Caspi
By: Danese, Andrea
.
Contributor(s): Moffitt, Terrie E | Arseneault, Louise | Bleiberg, Ben A | Dinardo, Perry B | Gandelman, Stephanie B | Houts, Renate | Ambler, Antony | Fisher, Helen L | Poulton, Richie | Caspi, Avshalom.
Material type: 
ArticleSeries: American Journal of Psychiatry.Publisher: Psychiatry Online, 2017Subject(s): CHILD ABUSE | ADVERSE CHILDHOOD EXPERIENCES | BRAIN DEVELOPMENT | CHILD DEVELOPMENT | CHILD EXPOSURE TO VIOLENCE | Dunedin Multidisciplinary Health and Development Study | LONGITUDINAL STUDIES | VICTIMS OF DOMESTIC VIOLENCE | NEW ZEALAND | UNITED KINGDOMOnline resources: Read abstract
In:
American Journal of Psychiatry, 2017, 174(4), 349-361Summary: Objective:
Individuals reporting a history of childhood violence victimization have impaired brain function. However, the clinical significance, reproducibility, and causality of these findings are disputed. The authors used data from two large cohort studies to address these research questions directly.
Method:
The authors tested the association between prospectively collected measures of childhood violence victimization and cognitive functions in childhood, adolescence, and adulthood among 2,232 members of the U.K. E-Risk Study and 1,037 members of the New Zealand Dunedin Study who were followed up from birth until ages 18 and 38 years, respectively. Multiple measures of victimization and cognition were used, and comparisons were made of cognitive scores for twins discordant for victimization.
Results:
Individuals exposed to childhood victimization had pervasive impairments in clinically relevant cognitive functions, including general intelligence, executive function, processing speed, memory, perceptual reasoning, and verbal comprehension in adolescence and adulthood. However, the observed cognitive deficits in victimized individuals were largely explained by cognitive deficits that predated childhood victimization and by confounding genetic and environmental risks.
Conclusions:
Findings from two population-representative birth cohorts totaling more than 3,000 individuals and born 20 years and 20,000 km apart suggest that the association between childhood violence victimization and later cognition is largely noncausal, in contrast to conventional interpretations. These findings support the adoption of a more circumspect approach to causal inference in the neuroscience of stress. Clinically, cognitive deficits should be conceptualized as individual risk factors for victimization as well as potential complicating features during treatment. (Authors' abstract). Record #5657
American Journal of Psychiatry, 2017, 174(4), 349-361
Objective:
Individuals reporting a history of childhood violence victimization have impaired brain function. However, the clinical significance, reproducibility, and causality of these findings are disputed. The authors used data from two large cohort studies to address these research questions directly.
Method:
The authors tested the association between prospectively collected measures of childhood violence victimization and cognitive functions in childhood, adolescence, and adulthood among 2,232 members of the U.K. E-Risk Study and 1,037 members of the New Zealand Dunedin Study who were followed up from birth until ages 18 and 38 years, respectively. Multiple measures of victimization and cognition were used, and comparisons were made of cognitive scores for twins discordant for victimization.
Results:
Individuals exposed to childhood victimization had pervasive impairments in clinically relevant cognitive functions, including general intelligence, executive function, processing speed, memory, perceptual reasoning, and verbal comprehension in adolescence and adulthood. However, the observed cognitive deficits in victimized individuals were largely explained by cognitive deficits that predated childhood victimization and by confounding genetic and environmental risks.
Conclusions:
Findings from two population-representative birth cohorts totaling more than 3,000 individuals and born 20 years and 20,000 km apart suggest that the association between childhood violence victimization and later cognition is largely noncausal, in contrast to conventional interpretations. These findings support the adoption of a more circumspect approach to causal inference in the neuroscience of stress. Clinically, cognitive deficits should be conceptualized as individual risk factors for victimization as well as potential complicating features during treatment. (Authors' abstract). Record #5657
