I had the privilege of attending another UCL Institute of Clinical Neuroscience seminar on Monday. This time, Prof. Ian Goodyer of the University of Cambridge came to talk to us about the neurobiology of Conduct Disorders.
I must admit, Conduct Disorder (CD) is a new one on me. Part of me wanted to just scoff and say “well, that’s just brattish children”, or maybe to suggest that it’s the early signs of a Personality Disorder (PD): neither is true. CD displays a range of very particular, severely anti-social behaviours, some of which are very similar to some PDs, but CD is particular to the 18-and-unders (children and adolescents). In to adulthood, people with CD may develop an antisocial PD, but it isn’t an accurate predictor: predicting later mental health issues from childhood behaviours is an incredibly difficult thing. Apparently, the greatest predictor of adult depression is NOT childhood depression, but irritability. Hence the need to differentiate between childhood and adult psychopathologies: a lot of brain development goes on as we grow, and our mental layout changes with it.
Psychiatrists also differentiate between two types of CD: Early Onset CD and Adolescent Onset CD. EO-CD presents in children under the age of about 10yrs, but seems to lessen with age. AO-CD on the other hand seems to occur as a learned behaviour, as individuals’ mimicry of already deviant peers: adolescents presenting AO-CD may not have had any sort of disorder when they were younger, but develop this in reaction to peergroups.
We already have evidence that patients presenting EO-CD have neuropsychological impairments, neurophysiological abnormalities and hormone abnormalities such as atypical cortisol levels (ahha! I know about cortisol now!) What Goodyer and his team have been researching is whether this is also true of AO-CD: if AO-CD is truly just mimicking behaviour based on peer-pressure or social affectation, and not based in neurophysiology. If AO-CD is truly distinct from EO-CD in this way, then patients presenting AO-CD should show similar test scores to normal controls on things such as empathy tests and so forth: they should not show the same scores as EO-CD. AO-CD and EO-CD, if truly different, should show distinct neurobiological characteristics.
But Goodyer and his colleagues have not found this: instead, AO and EO-CD both show similar results in empathy tests (i.e. they don’t seem to display much), they show similar responses to stress, both behaviourally and in terms of cortisol levels, and they both show similar problems in recognising facial expressions.
Goodyer has also run MRI scans for both groups and compared them to normal controls (he also had to go back and retest, after realising he would have to covary for ADHD). Again, both CD groups had very similar abnormalities in brain activity.
If EO and AO-CD are so similar in physiology and psychology, then why does AO-CD only emerge in adolescence? Why is it that EO-CD occurs early on, and AO-CD, statistically identical, doesn’t? This is proving a problem for the taxonomic theory. Perhaps something is preventing the onset of AO-CD in early childhood, or the reverse, that something is causing EO-CD to develop early. We’ve looked at the physiology, but perhaps what we need is a longitudinal study of environment – of course, this is fraught with ethical problems, but it looks to be the missing piece. Perhaps children susceptible to either form of CD are always going to be neurobiologically vulnerable, but depending on their upbringing and subsequent peer-groups, they may or may not actually exhibit any symptoms.
Image credits: from UCL website