Association of subcortical gray-matter volumes with life-course-persistent antisocial behavior in a population- representative longitudinal birth cohort | 2021
Carlisi, Christina O., Moffitt, Terrie E., Knodt, ... Show all » Annchen R., Harrington, HonaLee, Langevin, Stephanie, Ireland, David, Melzer, Tracy R., Poulton, Richie, Ramrakha, Sandhya, Caspi, Avshalom, Hariri, Ahmad R., Viding, Essi « Hide
Development and Psychopathology, 2021, 1-11.
10.1017/s0954579421000377
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Our ref: RO767
Show abstract » Neuropsychological evidence supports the developmental taxonomy theory of antisocial behavior, suggesting that abnormal brain development distinguishes life-course-persistent from adolescence-limited antisocial behavior. Recent neuroimaging work confirmed that prospectively- measured life-course-persistent antisocial behavior is associated with differences in cortical brain structure. Whether this extends to subcortical brain structures remains uninvestigated. This study compared subcortical gray-matter volumes between 672 members of the Dunedin Study previously defined as exhibiting life-course-persistent, adolescence-limited or low-level antisocial behavior based on repeated assessments at ages 7–26 years. Gray-matter volumes of 10 subcortical structures were compared across groups. The lifecourse- persistent group had lower volumes of amygdala, brain stem, cerebellum, hippocampus, pallidum, thalamus, and ventral diencephalon compared to the low-antisocial group. Differences between life-course-persistent and adolescence-limited individuals were comparable in effect size to differences between life-course-persistent and low-antisocial individuals, but were not statistically significant due to less statistical power. Gray-matter volumes in adolescence-limited individuals were near the norm in this population-representative cohort and similar to volumes in low-antisocial individuals. Although this study could not establish causal links between brain volume and antisocial behavior, it constitutes new biological evidence that all people with antisocial behavior are not the same, supporting a need for greater developmental and diagnostic precision in clinical, forensic, and policy-based interventions.
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