Mapping the structural organization of the brain in conduct disorder: replication of findings in two independent samples.

BACKGROUND: Neuroimaging methods that allow researchers to investigate structural covariance between brain regions are increasingly being used to study psychiatric disorders. Structural covariance analyses are particularly well suited for studying disorders with putative neurodevelopmental origins as they appear sensitive to changes in the synchronized maturation of different brain regions. We assessed interregional correlations in cortical thickness as a measure of structural covariance, and applied this method to investigate the coordinated development of different brain regions in conduct disorder (CD). We also assessed whether structural covariance measures could differentiate between the childhood-onset (CO-CD) and adolescence-onset (AO-CD) subtypes of CD, which may differ in terms of etiology and adult outcomes. METHODS: We examined interregional correlations in cortical thickness in male youths with CO-CD or AO-CD relative to healthy controls (HCs) in two independent datasets. The age range in the Cambridge sample was 16-21 years (mean: 18.0), whereas the age range of the Southampton sample was 13-18 years (mean: 16.7). We used FreeSurfer to perform segmentations and applied structural covariance methods to the resulting parcellations. RESULTS: In both samples, CO-CD participants displayed a strikingly higher number of significant cross-cortical correlations compared to HC or AO-CD participants, whereas AO-CD participants presented fewer significant correlations than HCs. Group differences in the strength of the interregional correlations were observed in both samples, and each set of results remained significant when controlling for IQ and comorbid attention-deficit/hyperactivity disorder symptoms. CONCLUSIONS: This study provides new evidence for quantitative differences in structural brain organization between the CO-CD and AO-CD subtypes, and supports the hypothesis that both subtypes of CD have neurodevelopmental origins.

Differential genetic and environmental influences on developmental trajectories of antisocial behavior from adolescence to young adulthood.

Little research has investigated differential genetic and environmental influences on different developmental trajectories of antisocial behavior. This study examined genetic and environmental influences on liabilities of being in life-course-persistent (LCP) and adolescent-limited (AL) type delinquent groups from adolescence to young adulthood while considering nonviolent and violent delinquency subtypes and gender differences. A genetically informative sample (n = 356, 15-16 years) from the first three waves of In-Home Interview of the National Longitudinal Study of Adolescent to Adult Health was used, with 94 monozygotic and 84 dizygotic pairs of same-sex twins (50% male). Biometric liability threshold models were fit and found that the male-specific LCP type class, chronic, showed more genetic influences, while the AL type classes, decliner and desister, showed more environmental influences. Genetic liability and shared environment both influence the persistence of antisocial behavior. The development of female antisocial behavior appears to be influenced more by shared environment.

Research review: evaluating and reformulating the developmental taxonomic theory of antisocial behaviour.

BACKGROUND: The developmental taxonomic theory proposes that there are two subtypes of antisocial behaviour. The first is a neurodevelopmental disorder which emerges in early childhood and follows a life-course persistent course, whereas the second emerges in adolescence, remits in early adulthood and reflects peer processes such as mimicry of antisocial peers. The aim of this review was to evaluate the developmental taxonomic theory in the light of recent empirical research. METHODS: We conducted a comprehensive literature review comparing these subtypes of antisocial behaviour based on searches on PubMed and other scientific databases covering the period from 1993 to 2013. We focused on research encompassing psychiatric epidemiology, personality assessment, neuropsychology, neuroendocrinology, genetics, and structural and functional neuroimaging. Sixty one empirical studies were identified that investigated one of these forms of antisocial behaviour separately or explicitly compared childhood-onset and adolescence-onset forms of antisocial behaviour. RESULTS: Empirical research provides support for the hypothesis that life-course persistent antisocial behaviour is a neurodevelopmental disorder which emerges in the transactions between individual vulnerabilities and environmental adversity. In contrast to the developmental taxonomic theory, however, empirical findings suggest that severe antisocial behaviour that emerges in adolescence frequently has a negative prognosis and is rarely limited to the adolescent period. In addition, both forms of antisocial behaviour are associated with emotion processing deficits, changes in brain structure and function, alterations in cortisol secretion, and atypical personality traits (such as increased callous-unemotional traits). CONCLUSIONS: We conclude that the developmental taxonomic theory is in need of revision, as differences between life-course persistent and adolescence-onset forms of antisocial behaviour appear to be quantitative, rather than qualitative, in nature. In addition, evidence is accumulating that adolescence-onset antisocial behaviour may also be a neurodevelopmental disorder. To account for the similarities between these groups, despite the differences in their age-of-onset, we propose that the quality of the child's early environment moderates the relationship between individual vulnerabilities and the age-of-onset of antisocial behaviour.

Regional Homogeneity Abnormalities in Early-Onset and Adolescent-Onset Conduct Disorder in Boys: A Resting-State fMRI Study.

Purpose: Developmental taxonomic theory posits that formation of early-onset conduct disorder (EO-CD), is considered to have a neurodevelopmental etiology and have more severe psychosocial and neuropsychological dysfunction than adolescent-onset CD (AO-CD), which is thought to stem largely from social mimicry of deviant peers. The purpose of the current study was to investigate whether regional homogeneity (ReHo), denoting the spontaneous brain activity, supports developmental taxonomic theory in a resting state (rs). Materials and Methods: Rs-functional magnetic resonance imaging (fMRI) examinations were administered to 36 EO-CD patients, 32 AO-CD patients, and 30 healthy controls (HCs). All participants were male adolescents, aged between 12 and 17 years old. A one-way analysis of covariance (ANCOVA), with age and IQ as covariates, was performed to identify regions with significant group differences in ReHo values, followed by a post hoc analyses. Results: Compared with the AO-CD groups, EO-CD had higher ReHo values in the right middle/inferior frontal gyrus. Compared with the HCs, the EO-CD group exhibited lower ReHo values in the left precuneus, left middle occipital gyrus, left cerebellum posterior lobe and the right inferior parietal lobule, as well as higher ReHo values in the right middle frontal gyrus, left insula/inferior frontal gyrus, right postcentral gyrus, and the left anterior cingulate gyrus. Compared with the HCs, the AO-CD group showed lower ReHo values in the bilateral precuneus, left cerebellum posterior lobe, and the right inferior parietal lobule. Conclusion: Significant differences in ReHo were observed between the EO-CD and AO-CD groups, implying distinct neuropathological mechanisms of the two CD subtypes, consistent with developmental taxonomic theory. CD-associated abnormalities in ReHo may be related to high-order cognitive and low-level perceptual system impairments in CD.

Cortical thickness, surface area, and folding alterations in male youths with conduct disorder and varying levels of callous-unemotional traits.

PURPOSE: Previous studies have reported changes in gray matter volume in youths with conduct disorder (CD), although these differences are difficult to interpret as they may have been driven by alterations in cortical thickness, surface area (SA), or folding. The objective of this study was to use surface-based morphometry (SBM) methods to compare male youths with CD and age and sex-matched healthy controls (HCs) in cortical thickness, SA, and folding. We also tested for structural differences between the childhood-onset and adolescence-onset subtypes of CD and performed regression analyses to assess for relationships between CD symptoms and callous-unemotional (CU) traits and SBM-derived measures. METHODS: We acquired structural neuroimaging data from 20 HCs and 36 CD participants (18 with childhood-onset CD and 18 with adolescence-onset CD) and analyzed the data using FreeSurfer. RESULTS: Relative to HCs, youths with CD showed reduced cortical thickness in the superior temporal gyrus, reduced SA in the orbitofrontal cortex (OFC), and increased cortical folding in the insula. There were no significant differences between the childhood-onset and adolescence-onset CD subgroups in cortical thickness or SA, but several frontal and temporal regions showed increased cortical folding in childhood-onset relative to adolescence-onset CD participants. Both CD subgroups also showed increased cortical folding relative to HCs. CD symptoms were negatively correlated with OFC SA whereas CU traits were positively correlated with insula folding. CONCLUSIONS: Cortical thinning in the superior temporal gyrus may contribute to the social cognitive impairments displayed by youths with CD, whereas reduced OFC SA may lead to impairments in emotion regulation and reward processing in youths with CD. The increased cortical folding observed in the insula may reflect a maturational delay in this region and could mediate the link between CU traits and empathy deficits. Altered cortical folding was observed in childhood-onset and adolescence-onset forms of CD.