Bad behaviour may be wired into adolescent brains early in life, according to a study which we published in the Journal of Child Psychology and Psychiatry. Young men with persistent behavioural problems, including destructive behaviour and lying and stealing, seem to have brains which differ significantly in structure from those of their better-behaved peers. We used MRI scans to look at the ‘map’ of male teenage brain and young adults who had been diagnosed with conduct disorder. This evidence now provides strong evidence of a link between serious antisocial behaviour and brain development.
As well as researchers at the University of Cambridge, researchers at the University of Southampton and the University of Rome “Tor Vergata” in Italy took part in this study which provides the clearest evidence to date that poor behaviour stems from changes in brain development in early life.
In particular, we looked at the coordinated development of different brain regions by studying whether they were similar or different in terms of thickness. Regions that develop at similar rates would be expected to show similar patterns of cortical thickness, for example. There’s evidence already of differences in the brains of individuals with serious behavioural problems, but this is often simplistic and only focused on regions such as the amygdala, which we know is important for emotional behaviour. But conduct disorder is a complex behavioural disorder, so likewise we would expect the changes to be more complex in nature and to potentially involve other brain regions.
For our study, which was funded by the Wellcome Trust and the Medical Research Council, we recruited 58 male adolescents and young adults with conduct disorder and 25 typically-developing controls, all aged between 16 and 21 years. We divided the individuals with conduct disorder according to whether they displayed childhood-onset conduct disorder or adolescent-onset conduct disorder. We found that youths with childhood-onset conduct disorder (sometimes termed ‘early-starters’) showed a strikingly higher number of significant correlations in thickness between regions relative to the controls. We believe this may reflect disruptions in the normal pattern of brain development in childhood or adolescence. On the other hand, youths with adolescent-onset conduct disorder (‘late starters’) displayed fewer such correlations than the healthy individuals. The researchers believe this may reflect specific disruptions in the development of the brain during adolescence, for example to the ‘pruning’ of nerve cells or the connections (synapses) between them.
As the findings were particularly striking, we wanted to replicate our findings in an independent sample of 37 individuals with conduct disorder and 32 healthy controls, all male and aged 13-18 years, recruited at the University of Southampton; this also confirmed the findings, adding to the robustness of the study. My colleague, Dr Graeme Fairchild, Associate Professor in Abnormal Psychology at the University of Southampton explains, “The differences that we see between healthy teenagers and those
with both forms of conduct disorders show that most of the brain is involved, but particularly the frontal and temporal regions of the brain. This provides extremely compelling evidence that conduct disorder is a real psychiatric disorder and not, as some experts maintain, just an exaggerated form of teenage rebellion.”
More research is now needed to investigate how to use these results to help these young people clinically and to examine the factors leading to this abnormal pattern of brain development, such as exposure to early adversity.
Although the findings point to the importance of the brain in explaining the development of conduct disorder, it is not clear how the structural differences arise and whether, for example, it is a mixture of an individual’s genetic make-up and the environment in which they are raised that causes the changes. However, these findings may make it possible to monitor objectively the effectiveness of interventions.